
Class. 
Book. 



Copyright N°_ 






COPYRIGHT DEPOSIT. 




Eye-ground in Arteriosclerosis 

(After de Sehweinitz) 



BLOOD-PKESSUKE 



ITS CLINICAL APPLICATIONS 



BY 

GEORGE WILLIAM NORMS, A.B., M.D. 

ASSISTANT PROFESSOR OP MEDICINE IN THE UNIVERSITY OP PENNSYLVANIA; VISITING PHYSICIAN 

TO THE PENNSYLVANIA HOSPITAL; ASSISTANT VISITING PHYSICIAN TO THE UNIVERSITY 

HOSPITAL; FELLOW OF THE COLLEGE OF PHYSICIANS OF PHILADELPHIA; 

MEMBER OP THE ASSOCIATION OF AMERICAN PHYSICIANS, ETC. 



SECOND EDITION, REVISED AND ENLARGED 



ILLUSTRATED WITH 102 ENGRAVINGS AND 1 COLORED PLATE 




LEA & FEBIGER 

PHILADELPHIA AND NEW YORK 
1916 



\9 



^ 



Entered according to the Act of Congress, in the year 1916, by 

LEA & FEBIGER, 
In the Office of the Librarian of Congress. All rights reserved. 




MAY 15 1916 
)GU431082 



f 



DEDICATED 
TO THE MEMORY OF 

FREDERICK A. PACKARD, M.D. 

WHOSE MEDICAL TALENTS AND KINDLY SPIRIT WERE UNTIMELY LOST TO 

THE COMMUNITY OF PHILADELPHIA, IN WHICH HE LIVED 

AT WHOSE SUGGESTION AND UNDER WHOSE GUIDANCE 

THE AUTHOR FIRST UNDERTOOK BLOOD-PRESSURE INVESTIGATIONS 

AND TO 
WHOSE SKILL AND SELF-SACRIFICING PROFESSIONAL CARE 

HE IN A LARGE MEASURE OWES HIS LIFE. 



PREFACE TO THE SECOND EDITION. 



The exhaustion of the first edition of this work in considerably 
less than two years after publication is a source of gratification and 
pleasure to the author. In the process of revision for the second 
edition an increase in size has been necessary in order to include a 
survey of the constantly growing literature on blood-pressure. 

The author has continued his endeavor to present the subject of 
blood-pressure in a condensed and practical form as definitely as 
the present state of our knowledge permits. Wherever possible, 
a summary of the experimental as well as the clinical data available 
for the consideration of a given topic has been included, together 
with references to articles upon which statements are based. 

As in the earlier edition the chapters upon Physiology and upon 
Venous Blood-pressure were written by Dr. J. Harold Austin, to 
whom the author is also indebted for assistance in the preparation 
of the chapter dealing with the Functional Efficiency of the Circu- 
lation. The author's thanks are also due to Miss Eleanor A. Cantner 
for valuable assistance in the preparation of the charts and drawings, 
as well as in proof reading. 

G. W. N. 
1530 Locust St., 
Philadelphia, 191(5. 



CONTENTS. 



CHAPTER I. 
The Physiology of Blood-pressure 17 

CHAPTER II. 

The Instrumental Estimation of Blood-pressure 58 

CHAPTER III. 
The Instrumental Estimation of Blood-pressure (Continued) 83 

CHAPTER IV. 
Venous Blood-pressure 135 

CHAPTER V. 

The Functional Efficiency of the Circulation as Determinable 

by Blood-pressure Estimation and Allied Tests .... 145 

CHAPTER VI. 

Arterial Hypotension 185 

CHAPTER VII. 
Blood-pressure in Acute Infectious Disease 196 

CHAPTER VIII. 
Blood-pressure in Chronic Infectious Disease 213 

CHAPTER IX. 
Exogenous Intoxications 225 

CHAPTER X. 
Blood-pressure in Cardiac Disease, Etc 233 



CONTENTS vill 

CHAPTER XI. 
Blood-pressuiie in Arteriosclerosis — Vascular Crises .... 250 

CHAPTER XII. 

Arterial Hypertensive Cardiovascular Disease, Nephritis, Etc. 266 

CHAPTER XIII. 
The Treatment of Arterial Hypertension 299 

CHAPTER XIV. 

Effects of Drugs and Glandular Extracts on Blood-pressure 

(Arranged Alphabetically) 324 

CHAPTER XV. 
Metabolic Diseases and Miscellaneous Conditions 347 

CHAPTER XVI. 

Diseases of the Nervous System . 369 

CHAPTER XVII. 

Blood-pressure in Surgery and Obstetrics 376 

CHAPTER XVIII. 
Ophthalmology • ■ 402 



A CLINICAL STUDY OF BLOOD-PRESSORE. 



CHAPTER I. 
THE PHYSIOLOGY OF BLOOD-PRESSURE. 

By J. HAROLD AUSTIN, M.D. 

Definitions. — Blood-pressure is the term used to indicate the 
pressure exerted by the blood at a given point in the circulatory 
system at a given moment. Thus we may speak of intra-auricular, 
intraventricular, arterial, capillary, or venous blood-pressure. When 
not qualified, the term is used to refer to the arterial blood-pressure, 
and in man usually to the pressure in the' brachial artery. The 
arterial blood-pressure is constantly undergoing rhythmic fluctua- 
tions due to the cardiac systoles. The highest pressure attained 
during one cardiac cycle is called the systolic pressure and is attained 
at the moment of the arrival of the crest of the pulse wave. The 
lowest pressure attained during a cardiac cycle is called the diastolic 
pressure. The difference between these two pressures is called the 
pulse pressure. Thus, if the systolic pressure be 120 and the diastolic 
90, then the pulse pressure would be 30. By mean pressure is under- 
stood the average pressure at a given point. The mean pressure 
is not, however, the arithmetical mean between the systolic and 
diastolic pressures, because the pressure may remain for only a 
moment at the systolic level, falling very quickly to near the diastolic 
level and remaining near it throughout the greater part of the 
average cycle. This is illustrated in the accompanying diagram in 
which obviously the average pressure lies much nearer to the 
diastolic than to the systolic. 

In addition to the pressure oscillations, dependent upon the cardiac 
cycle and called oscillations of the first order, there are slower oscil- 
lations in the arterial pressure dependent upon the respiratory 
movements. These are called blood-pressure oscillations of the 
second order. Finally, still slower oscillations, usually over ten to 
2 



18 



THE PHYSIOLOGY OF BLOOD-PRESSURE 



twenty cardiac cycles, occur. These are due to various factors, 
among which rhythmic variations in the activity of the vasocon- 
strictor centre or in the cardiac activity are the most important. 
These constitute the oscillations of the third order. All three types 
of oscillations are shown in the tracing (see Fig. 6). 




Fig. 1.- 



-S = systolic pressure ; D = diastolic pressure ; 
average pressure. 



M 



The pressure which is exerted by the blood against the vessel 
wall while the current flows unobstructed through the vessel is 
known as the lateral pressure. The pressure exerted by the blood 
against an obstruction in the lumen of the vessel is known as the 
end pressure. The end pressure exceeds the lateral pressure at any 
given point, and the difference is the pressure that is effective in 
producing the blood-flow at that point. The accompanying diagram 




Fig. 2. — Illustrating lateral pressure: 1, 2, 3, 4, 5, lateral pressure at points along 
outflow tube; h, the difference between lateral pressure and end pressure at any point. 
(From Howell.) 



(Fig. 2) illustrates the relation between lateral and end pressures. 
End pressure in a branch artery is shown to be approximately 
equal to the lateral pressure in the mam trunk at the point at 
which the branch takes origin. The method used commonly for 
the measurement of blood-pressure in man shows the end systolic 



METHODS OF MEASUREMENT 



19 



pressure in the brachial artery and the lateral diastolic pressure. 1 
Blood-pressure is usually expressed in millimeters (sometimes 
centimeters) of mercury above or below the atmospheric pressure 
at the same point. Thus blood-pressure of 120 is a pressure that 
will sustain in addition to the atmospheric pressure at the point, 
the pressure of a vertical column of mercury 120 mm. high. 




Fig. 3. — M, mercury manometer; F, float; G, perforated cap; P, recording pen; 
C, cannula for insertion into vessel; w, washout tube, shown in detail at B; R and 
E, for introduction and outflow of magnesium sulphate solution; both are clamped 
off while recording pressures. (From Howell.) 

Methods of Measurement. — The first exact measurements of blood- 
pressure were published by the Rev. Dr. Stephen Hales, an English- 
man, in a little book entitled Statical Essays, in 1733. He meas- 



'A. K. Cushny, Zentralbl. f. Physiol., Leipsic u. Wien, 1907-8, xxi, 77; N. D. 
Straschesto, Archiv f. d. ges. Physiol., Bonn, 1909, cxxviii, 1. 



20 THE PHYSIOLOGY OF BLOOD-PRESSURE 

ured the pressure in the femoral artery of a horse by connecting 
it with a glass tube and noting the height to which the blood rose 
in this tube held vertically. In 1828 Poiseuille applied the mercury 
manometer to the study of blood-pressure and in 1847 Ludwig 
invented the recording manometer with moving drum. Ludwig's 
method is essentially the one used today in physiological experi- 
ments. A manometer is connected by tubing filled with some 
fluid which will inhibit coagulation, such as saturated magnesium 
sulphate solution, with a cannula introduced into the artery. A 
manometer so connected gives a record of the end pressure in the 
artery. 

In physiological work the mean pressure is obtained by con- 
stricting the communication between the manometer and the vessel 




Fig. 4. — Diagram of Hiirthle manometer. Tubing from heart or vessel to small 
tambour T, both filled with fluid. Movements of tambour magnified by compound 
lever S, and transmitted to writing pen. (From Howell.) 

to a small opening. This prevents the transmission of the faster 
blood-pressure oscillation to the manometer, and leads to the pro- 
duction of a straight line representing the average or mean pressure. 
In studies upon man the mean pressure cannot thus be directly 
recorded and is, in fact, difficult to determine. All pressures deter- 
mined upon human beings are therefore, as a rule, either systolic or 
diastolic pressures. It is the custom of some authors to speak of 
that pressure which is half-way between the systolic and diastolic 
pressures in man as the mean pressure. This seems to us misleading, 
inasmuch as it may in certain cases be considerably above the true 
mean pressure. Dawson 1 has shown that the mean pressure in 
man is usually obtained by adding approximately one-third of the 

1 Brit. Med. Jour., 1906, ii, 996. 



METHODS OF MEASUREMENT 



21 



pulse pressure to the diastolic pressure. For the measurement of 
the systolic and diastolic pressures in physiological work, Hurthle 
devised the membrane manometer which is shown in Fig. 4, since 
the inertia of the column of mercury in the mercury manometer 
is too great to give an accurate record of the rapid fluctuations. 




To the artery 



Fig. 5. — Maximum-minimum manometer. When cock a is open and b closed, the 
highest pressure attained during the period of record is transmitted to the manometer 
and retained by the maximum valve. When a is closed and b opened, the mercury 
falls to the lowest pressure occurring in the period of record and is retained there by 
the minimum valve. 



Another method in use in physiological work for the control of the 
membrane manometer is the so-called valve manometer, or maximal- 
minimal manometer. This is illustrated in Fig. 5. By using one 
valve or the other, either the highest or the lowest pressure occur- 
ring within a given interval of time is recorded. The maximal press- 



22 



THE PHYSIOLOGY OF BLOOD-PRESSURE 



ure recorded by such a manometer is not, however, identical with 
the systolic pressure, nor the minimal with the diastolic pressure. 
This may be seen by referring to Fig. 6. The maximal-minimal 
manometer will record the highest or lowest pressure attained over 
a certain period of time, and this is usually long enough to admit 
the occurrence of all three orders of pressure oscillations. It would 



i n mmin 1 1 1 1 1 1 1 1 1 i i n 1 1 i i i 1 u nin \ i it i 1 1 1 n 1 1 1 mm i n n n i 



rWtAA/v/W^ v ^ATMAr vv ,/^/'A 



<vVv 



Base Line 



110 



80 



60 



40 



20 mm 



Babbit 



Fig. 6. — Diagram illustrating at Bp a typical blood-pressure curve dampened by 
constricting the communication between the artery and the manometer so as to 
reduce the amplitude of the shortest waves. Shortest waves, cardiac; longer waves, 
respiratory; longest waves (three in the tracing), waves of third order. T, time 
record in seconds. (From Howell.) 



seem desirable, therefore, to use the terms maximal and minimal 
pressures in this sense. Certain authors, however, have used these 
terms as synonymous with systolic and diastolic pressures respec- 
tively. 

Measurements of the blood-pressure in the smaller arterioles 
and capillaries either in man or in animals must be made by other 
methods, and are described in a later chapter. 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 23 

Venous pressure is measured, in physiological work, in the same 
way as the arterial, but usually with a water manometer rather 
than with a mercury manometer. A pressure of 34 cm. II 2 is 
equal to a pressure of 25 mm. Hg. Blood-pressure within the heart 
is measured by introducing an oiled cannula, either through one of 
the vessels or through a puncture wound, into the chamber within 
which the pressure is desired. 

BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE. 

The blood-pressure in an individual varies with the point of the 
cardiovascular system under consideration, its elevation with 
respect to the heart, and with the phase of the heart, whether systole 
or diastole. These variations are indicated in Table I, which gives 
approximate systolic and diastolic pressures in different parts of 
the cardiovascular system at the level of the heart in man. That 
the blood-pressure varies greatly in different parts of the vascular 
system has long been known, the marked difference in the force of 
the stream flowing from a cut artery and from a cut vein being a 
striking illustration. 

Table I. — Approximate Pressure in Cardiovascular Tree op a Normal 
Man, Aged Twenty Years, at Level op Heart. 

In mm. Hg. 
Systolic. Diastolic. 

Left ventricle 150 to 200 

Aorta 150 to 200 100 to 120 

Brachial artery 105 to 140 80 to 110 

Radial artery 95 to 125 

Arterioles 80 to 95 

Medium capillaries 50 to 60 50 to 60 

Smallest capillaries 20 to 35 20 to 35 

Smallest veins 20 to 30 20 to 30 

Large vein of arm 1 to 15 1 to 15 

Right ventricle 25 to 60 

Pulmonary artery 25 to 60 15 to 25 

This table is extremely diagrammatic and is intended merely to 
emphasize certain facts. It will be noted that the chief fall in 
pressure occurs between the smaller arteries and the capillaries, 
that is, in the arterioles; furthermore, that this affects the systolic 
pressure more than the diastolic, so that under normal conditions 
the pressure in the capillaries shows no pulse wave. When the 
arterioles are widely dilated this fall of pressure, especially of systolic 
pressure, in them is diminished and an appreciable pulse may 
penetrate into the capillaries. Under these conditions the systolic 



24 THE PHYSIOLOGY OF BLOOD-PRESSURE 

pressure in the capillaries approaches that in the smaller arteries, 
and the diastolic pressure in the arteries approaches that of the 
capillaries. It will further be noted that any increase in venous 
pressure must promptly elevate the capillary pressure. Indeed, 
the capillary pressure is more readily raised by venous stasis than 
by increased arterial pressure. 

In the recumbent position the lateral pressure throughout the 
entire length of the aorta is very nearly constant. In the upright 
position, however, the pressure at the lower end of the aorta is 
higher than the pressure at the arch, by the weight of the column of 
blood separating the two points; approximately 2 mm. Hg. per inch. 

In the veins the pressure is largely dependent upon posture, 
i. e., upon the height of the point measured above or below the right 
auricle. At the right auricle the pressure is probably about to 10 
mm. Hg., varying with the phase of respiration, and that in the trunk 
is about 2 mm. higher for every inch below the heart; in the lower 
extremities, however, the venous pressure, while high, is not so 
high as this calculation would indicate (see p. 135). This relation 
leads to some distention of the veins in the lower and dependent 
portions of the body, while the veins of the upper portion of the 
body are but partially filled. 

The Factors that Maintain and Regulate Blood-pressure. — The 
cardiovascular system may be considered from this point of view 
as consisting of six elements. (1) The heart, the source of energy. 
(2) The arteries acting as elastic vessels, dilating to receive each 
new ventricular delivery of blood, and contracting to maintain 
during the filling and resting periods of the heart an even flow 
through the capillaries. (3) The capillaries, the site of active 
functionation of the blood and with the smaller arterioles the chief 
source of the resistance in the circulation. (4) The veins which 
with the capillaries serve as a reservoir, maintaining a pressure 
just sufficient to fill promptly the relaxing heart for its next systolic 
contraction. (5) The blood itself, the incompressible, inelastic 
medium which fills the cardiovascular system. (6) The lymphatic 
system with its tissue spaces, serous cavities and lymphatic chan- 
nels filled with lymph, acting as an additional but less promptly 
available reservoir for body fluids. 

The Heart. — The heart is the chief source of the energy that 
maintains the blood-pressure. The factors that affect the heart's 
efficiency to this end are the factors that influence the output of 
blood per minute from the heart. They are as follows: (1) The 






BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 25 

diastolic filling of the ventricles; this is dependent upon (a) the 
venous pressure, (b) the length of diastole, and (c) the cardiac tone. 
(2) The completeness of systolic emptying. (3) The number of 
beats per minute, or cardiac rate. (4) The efficiency of the valves 
of the heart. The cardiac cycle may be divided into two parts: 
(1) systole, or the period of cardiac contraction, (2) diastole, or 
the period of cardiac relaxation and rest. The ventricular systole 
and diastole are each further subdivided. The first one-third or one- 
fourth of the ventricular systole is occupied in raising the pressure 
within the ventricle, from the pressure produced by the auricular 
systole to the diastolic pressure of the pulmonary artery or of the 
aorta. This is the so-called presphygmic period or " anspannungs- 
zeit." When this pressure is attained the semilunar valves open 
and, with the propulsion of the blood onward into the aorta, the 
pressure rises in both ventricle and aorta to the systolic pressure. 
This pressure is then maintained in the ventricle almost to the end 
of systole, driving the blood at an even rate out into the aorta and 
into the smaller vessels. With the relaxation at the close of systole 
the pressure in the ventricles falls to zero as the semilunar valves 
close. Diastole now commences. The venous pressure causes the 
tricuspid and mitral valves to open and the blood fills the ventricles 
at a rate dependent upon the venous pressure. The amount of 
distention produced in the ventricle by a given venous pressure is 
determined by the cardiac tone — the greater the tone, the less the 
distention. When this inflow is completed the diastole proper ends 
and the remainder of the cycle is occupied by a period of rest or 
diastasis. 

With changes in cardiac rate, the duration of both systole and 
diastole are altered, but the former much less than the latter. The 
length of the systole in man, with a pulse rate of about 75 to 95, 
is from 0.3 to 0.38 second. With slow rates that permit time for 
adequate filling of the ventricles Henderson, 1 Bohr 2 and Putter 3 
have found that providing an adequate venous pressure is main- 
tained, the systolic discharge is under normal conditions practically 
a constant quantity for any given individual, and the changes in 
the rate influence only the duration of diastasis. Hence the cardiac 
output per minute under such conditions will be proportional to 
the cardiac rate. With a more accelerated pulse rate, however, 

1 Am. Jour. Physiol., 1912-13, xxxi, 288, 352, 399. 

2 Skand. Arch. f. Physiol., 1909, xxii, 221. 
3 Ztschr. f. klin. Med., 1911, lxxiii, 342. 



26 THE PHYSIOLOGY OF BLOOD-PRESSURE 

Henderson has shown that the ventricle has not sufficient time to 
receive its full quota of blood and the diastole is shortened. In 
consequence, the systolic discharge is diminished, and although the 
volume output per minute still increases as the pulse becomes 
more rapid, it falls farther and farther behind proportionally. Hen- 
derson holds to the view that the systolic output of the heart is 
determined entirely by two factors — the cardiac rate, altering the 
duration of the diastole, and the venous pressure. On the other 
hand, Zuntz 1 and Plesch 2 find evidence to support the view that, 
in addition, the heart is capable of varying its output per minute 
independently of the rate and of the venous pressure, as the result 
of direct changes in the cardiac tonus and in the amplitude of the 
cardiac stroke. 

Henderson and Barringer have found that with normal cardiac 
tonus the venous pressure necessary to distend the right ventricle 
as rapidly as it relaxes is not more than 5 mm. of water in excess 
of the intrathoracic pressure. This he calls the critical venous 
pressure. Studies upon the dog and man have led him to the view 
that while normally the pressure in the intrathoracic veins may dur- 
ing a very deep inspiration become less than atmospheric, it never 
normally becomes less than 45 mm. of water above the intrathoracic 
pressure and therefore falls scarcely, if at all, below the critical 
pressure. In normal inspiration, the descent of the diaphragm, by 
compressing the abdominal capillaries and veins, somewhat increases 
the venous flow into the thorax. 

In an athlete, panting after a contest, not only the inspiratory 
descent of the diaphragm, but also the powerful expiratory con- 
traction of the abdominal muscles must hasten the venous flow 
from the splanchnic area to the right auricle, and aid in maintain- 
ing the critical venous pressure in spite of the accelerated cardiac 
rate and hence increased cardiac output. It is probable that in 
extreme tachycardia, the shortening of diastole and consequent 
imperfect filling of the ventricle may actually lead to a diminished 
cardiac output per minute. 

Henderson and Prince 3 from a study of the oxygen pulse (the 
oxygen consumption by the body per minute divided by the pulse 
rate) with varying amounts of work, have concluded that the 
systolic discharge of a well-developed man, working hard and with 
a pulse rate of 140 per minute, is not less than 100 c.c. of blood. 

i Ztschr. f. klin. Med., 1912, lxxiv. 347. 2 Ztschr. f. Physiol., 1912, xxvi, 90. 

s The Oxygen Pulse and the Systolic Discharge, Am. Jour. Physiol., 1914, xxxv, 106. 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 27 

Venous Pressure. — So long as an adequate venous pressure is 
maintained, the cardiac output per beat is probably dependent 
upon the duration of diastole. x\t slow and normal cardiac rates, 
the diastolic filling is complete, but at accelerated rates the filling 
becomes progressively diminished. Inadequate venous pressure 
reduces the cardiac output. On the other hand, in the presence of 
a dilated heart an abnormally high venous pressure probably 
tends to keep the ventricles overdistended, thus establishing a 
vicious cycle. 

Cardiac Rate. — At slow and moderate rates the cardiac output 
per minute is probably proportional to the cardiac rate. At more 
rapid rates the minute output increases with the pulse rate, but not 
proportionally. At extremely rapid rates imperfect ventricular 
filling may probably actually diminish the minute output. 

We may sum up the effects of these factors as follows: 

Cardiac Tone. — Either unduly diminished cardiac tone, by per- 
mitting dilatation of the ventricles, or unduly increased cardiac 
tone, by interfering with the diastolic filling, impairs the cardiac 
output. 

Stenotic or incompetent valves tend to diminish the cardiac 
output, although this defect is at first compensated by increased 
amplitude of contraction and frequently by increased rate. 

Of these various factors, changes in one may to some extent be 
compensated by changes in another. Elevation of venous pressure 
may be counteracted by increase of cardiac tone. On the other 
hand, no changes in cardiac activity can compensate a deficient 
venous return resulting from hemorrhage, from stagnation of the 
blood in the widely dilated peripheral vessels (vasomotor shock), or 
from some mechanical obstruction to the venous flow. The reflex 
acceleration of the cardiac rate that results is usually ineffective. 

Marey noted that increased blood-pressure is followed by slow- 
ing of the pulse, and later Eyster and Hooker 1 showed that this 
is due to vagus stimulation occurring reflexly when the blood- 
pressure in the carotids or the aorta is increased, even though 
changes in the cerebral circulation be excluded. The action of the 
vagus upon the heart is to diminish the cardiac rate by reducing 
the activity of the "pace-maker," and therefore to decrease the 
output per minute, and when extreme, to reduce the conductivity 
of the auriculoventricular bundle, producing partial or complete 
block. 

1 Zentralbl. f. Physiol., Leipsic u. Wien, 1907, xxi, 615. 



28 THE PHYSIOLOGY OF BLOOD-PRESSURE 

Roy and Adami 1 have shown by cardiometer studies that with 
increased aortic pressure, even though the output per minute may 
be increased, the residual blood (that remaining in the ventricles 
at the end of systole) is increased and the ventricles become more 
widely dilated during diastole. Excessive aortic pressure therefore 
leads to loss of ventricular tone, with dilatation and impairment of 
cardiac efficiency. 

Arteries. — The elasticity of the arteries, by virtue of which they 
dilate during each systole to accommodate the ventricular output 
with only a moderate rise of the pressure within them, and then 
during diastole contract again, forcing a continuous stream through 
the capillaries and maintaining under normal conditions a fair 
pressure throughout diastole, is a property of the utmost importance. 
Without this elasticity the strain upon the cardiac muscle would be 
enormously increased, as would be the strain during systole upon 
the vessel walls. Were the heart pumping into an absolutely rigid 
system, the cardiac systole would be prolonged, the systolic pressure 
enormously increased and the diastolic pressure would fall to zero, 
with a cessation of flow during diastole. The pulse pressure would 
equal the systolic pressure. Such an extreme condition never 
actually exists, but some approach toward it may be seen in indivi- 
duals with sclerotic arteries in whom often a systolic pressure of 
200 may be associated with a diastolic pressure of 130; a pulse press- 
ure, therefore, of 70, as contrasted with the normal pulse pressure of 
about 30. Obviously this exaggeration of the pulse pressure by 
rigid vessels will be less marked if the cardiac rate be increased and 
the output per beat correspondingly diminished. The pulse pressure 
is not infrequently looked upon as a rough measure of the cardiac 
activity. This to some extent it is; yet we have just seen it is 
influenced also to a marked degree by the condition of the arteries. 
It has been commonly accepted that this elasticity of the arteries, 
while it results from the tonus of their muscular coats, is to be looked 
upon as a passive elasticity not unlike that of a rubber tube. Hase- 
broek 2 has, however, recently advanced the hypothesis that while 
the dilatation of the arteries is a passive result of the injected volume 
of blood, their contraction is an active muscular act and, indeed, an 
important adjunct to the heart in the maintenance of blood-pressure 
and blood-flow. He believes this active arterial contraction to be 
the chief cause of the dicrotic wave of the sphygmogram. 

1 British Med. Jour., 1SSS, ii, 321. 

2 Deutsch. Archiv f. klin. Med.. 1911, eii, 567. 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 29 

Arterioles, Capillaries, and Veins. — The smaller arterioles together 
with the capillaries constitute the main resistance in the circulation, 
and are chiefly responsible for the proper distribution of the blood- 
flow to various organs and tissues, as the relative demands of these 
for blood changes with altering activity. The blood which reaches 
the smaller arterioles at a mean pressure, but little below that in 
the aorta, leaves them at a very low pressure, varying with the 
portion of the body under consideration. Whether this fall of 
pressure occurs chiefly in the small arterioles or in the capillaries 
is a matter of dispute. The capillaries together with the veins of 
the body serve as a reservoir for the blood. Complete loss of tone 
in these vessels leads to the accumulation in them, particularly in 
the splanchnic region, of practically all the blood in the body. The 
capillary and venous tone is therefore responsible for maintaining 
the supply of blood to the right auricle and this, as we have already 
seen in considering the heart, is of the utmost importance for the 
maintenance of cardiac output and of blood-pressure. 

The Vasomotor System. — In this relation it is the capillaries and 
veins of the splanchnic area that are of greatest significance. This 
was shown experimentally by Ludwig and Thiry 1 in 1864. These 
vessels alone are capable of containing all the blood of the body and 
were they to lose their tone the individual would promptly " bleed 
to death in his own vessels," as in vasomotor shock. In certain of 
the lower animals the tone of these vessels is relatively low. The 
hutch rabbit can be killed by simply holding it by the ears in the 
vertical position, the splanchnic vessels not having sufficient tone 
to overcome the force of gravity. In the dog manual pressure over 
the abdomen will cause a prompt rise of carotid blood-pressure of 
20 or 30 mm. of mercury due to the forcing of the blood from the 
vessels onward to the right auricle. The regulation of the tone 
of the arterioles, capillaries, and perhaps veins, is the most impor- 
tant factor toward this end. This is brought about by the vaso- 
motor nervous system. The vasomotor system consists of two main 
parts, the vasoconstrictor system and the vasodilator system. 

The Vasoconstrictor System. — The first important experimental 
studies upon this subject were those of Claude Bernard. 2 In 1851 
he noted the dilatation of the vessels in the ear of the rabbit after 
cutting its cervical sympathetic nerve on the same side. Later he 

1 Quoted by Howell, Text-book of Physiology, Philadelphia, 1912; Sitz. d. kais. 
Akad. d. Wiss. math, naturw. CI., 1864, xlix, 2, p. 442. 

2 Legons sur les liquides de l'Organisme, Paris, 1859. 



30 THE PHYSIOLOGY OF BLOOD-PRESSURE 

observed that electrical stimulation of the upper end of the cut 
nerve caused constriction of these dilated vessels. Thus was demon- 
strated the existence of vasoconstrictor nerves. 

The vasoconstrictor system consists of a centre in the medulla 
which is connected with the vessels of the body by nerve paths, each 
consisting of three neurons. In the medulla beneath the middle 
of the fourth ventricle exists the bilateral nerve centre which is 
chiefly responsible for the maintenance of vasomotor tone. This 
centre is continuously in a state of tonic activity which at times 
undergoes rhythmic fluctuations, giving rise to the Traube waves, 
to be described. Porter has recently found evidence against the 
view that both the arterial tonus and the vasomotor reflexes follow- 
ing stimulation of afferent nerves are controlled by the same master 
cells, the so-called vasomotor centre. He has been able by the use 
of curare in cats to more than double the sciatic and the depressor 
reflex change in blood-pressure, while the arterial tonus is left sub- 
stantially unchanged. Possibly, therefore, we may be compelled 
to recognize two centres, a vasotonic and a vasoreflex centre, related 
but separable. 1 The axons leading from these medullary cells 
pass down the cord to end around cells of the anterior horn, from 
the upper thoracic level to the upper lumbar, and constitute, with 
the medullary cell, the first neuron. The axons of the anterior horn 
cells are medullated and constitute the second neuron in the chain, 
the so-called preganglionic fibers. They pass from the cord in the 
white rami communicantes from the first thoracic to the second or 
fourth lumbar segments, and entering the sympathetic chain, have 
one of three destinations. Those destined for the extremities end 
around cells in the sympathetic chain. The non-medullated fibers 
of these sympathetic cells constitute the third neuron, the post- 
ganglionic fibers. They pass by the gray rami communicantes back 
to the spinal cord and thence accompany the appropriate spinal 
nerves to their destination. The preganglionic fibers destined for 
the deeper vessels of the head pass through the white rami of the 
first to sixth thoracic segments and up the sympathetic to the 
superior cervical ganglion. From this point the associated postgan- 
glionic fibers are distributed through the carotid and other vascular 
plexuses. The preganglionic fibers destined for the vessels of the 
abdominal and pelvic viscera, the most important of all in the 
regulation of blood-pressure, pass directly through the sympathetic 

1 Am. Jour. Physiol., 1914-15, xxxvi, 418. 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 31 

chain and by way of the splanchnic nerves to the celiac, inferior 
mesenteric, or other large prevertebral ganglia. From these ganglia 
the postganglionic fibers are distributed to the plexuses around the 
abdominal vessels. Section of the first neuron in this chain, as by 
section of the cervical cord, leads to extreme loss of vascular tone 
with fall in blood-pressure, failure of the circulation, and death. If 
the circulation be, however, artificially maintained after section of 
the cervical cord, the spinal cells, the second neurons, gradually 
assume a moderate tonic activity and restore a very imperfect vas- 
cular tone. This may in turn be destroyed by destruction of the 
spinal cord. Finally, Goltz 1 has shown that even after destruction 
of the cord, some vascular tone may be recovered which must be 
attributed to tonic activity either of the third postganglionic 
neuron or of the musculature of the vessel wall. Excitation of the 
vasoconstrictor centre with contraction of the peripheral vessels 
is called forth by the stimulation of pressor fibers, which may be 
demonstrated in almost any large nerve containing afferent fibers, 
but especially in the cutaneous nerves. These pressor fibers may 
be stimulated by electricity, by cold applied to the skin, and in 
other ways. Depression of the centre with diminished contraction 
of the vessels is called forth by stimulation of other afferent fibers, 
called depressor fibers. These likewise may be demonstrated in 
many of the large afferent nerves. Thus, application of warmth 
to the skin leads to local vascular dilatation, the result of stimulation 
of depressor fibers. Sensory stimuli from certain regions, notably 
the middle ear and the testis, give rise, as a rule, to depressor effects. 
Electric stimulation of the central end of the cut sciatic or of the 
splanchnic nerve may lead to either pressor or depressor effects. 

Since mental work or especially mental interest leads to a constric- 
tion of the bloodvessels with a rise of blood-pressure, it seems 
likely that pressor and probably also depressor fibers pass from the 
cortical centres to the vasoconstrictor centre. Medullary anemia 
and increased C0 2 concentration of the medullary blood are both 
potent stimulants to the vasoconstrictor centre. Many drugs exert 
a direct effect upon this centre. Ludwig and Cyon, 2 in 1866, demon- 
strated in the rabbit the so-called depressor nerve of the heart. 
This is an afferent nerve running in the sheath with the vagus, or 
in other species forming a part of the vagus. Stimulation of its 
peripheral cut end is without effect, but of its central end, leads to 

1 Arch. f. d. gesamt. Physiologie, 1896, lxiv, 397. 

2 Bericht d. sachsisch. Gesellsch. d. Wissensch. math. Phys. CI., 1866, p. 315. 



32 THE PHYSIOLOGY OF BLOOD-PRESSURE 

depression of the vasomotor centre and stimulation of the cardio- 
inhibitory centre, tending to lower blood-pressure. It is supposed 
to exert a steadying effect upon blood-pressure and to be stimulated 
mechanically by increase of aortic pressure. The older view that it 
was stimulated chiefly by intraventricular pressure has been ren- 
dered improbable by the work of Eyster and Hooker. 1 Einthoven 2 
has found an impulse passing up this nerve with every cardiac beat. 

The Vasodilator System. — It was likewise Claude Bernard 3 who 
first recognized the existence of vasodilator nerves. He noted that 
stimulation of the peripheral end of the cut chorda tympani nerve 
caused great dilatation of the bloodvessels of the submaxillary gland, 
with increased flow through the afferent vein ; this vein in some cases 
actually pulsated. Dilator fibers have been demonstrated in certain 
of the cranial nerves and in the sympathetic chain. The chorda 
tympani conveys such fibers from the facial nerve for distribution 
to the submaxillary and sublingual glands and the anterior two- 
thirds of the tongue. The glossopharyngeal nerve carries such fibers 
to the posterior third of the tongue, the tonsils, pharynx, and 
parotid gland. 

From the cervical sympathetic dilator, fibers pass to the lips, 
gums, palate and skin of the face, passing through the Gasserian 
ganglion and thence with the fifth nerve. From the thoracic sym- 
pathetic dilator, fibers pass through the splanchnic nerves to the 
abdominal viscera. From the first to third sacral segments of the 
cord dilator, fibers pass to the hypogastric plexus, whence as the nervi 
erigentes they supply the penis, and when stimulated cause erection. 
The existence of dilator fibers to the limbs, first upheld by Goltz, 
has been rendered uncertain by the work of Bayliss. 4 Both types of 
efferent fibers, vasoconstrictor and vasodilator, may exist in the 
same nerve, for example, in the splanchnic. As a rule these fibers 
react to different types of electrical stimulation, the dilators 
responding to weaker and to more slowly interrupted currents, 
responding less promptly, and once having done so, showing a 
more prolonged reaction than do the constrictor fibers. Moreover, 
a few days after section of such a nerve the irritability of the con- 
strictor fibers is lost, while that of the dilators is still retained. 

There is no evidence that there exists one general vasodilator 
centre associated with the dilator nerves, but rather that there are 
many centres through the cerebrospinal axis for the various areas 

1 Loc. cit. - Quoted by Howell. 3 Loc. cit. 

1 Jour, of Physiol., 1900, xxvi, 173; ibid., 1902, xxviii, 276. 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 33 

supplied. Probably the vasodilator system is of less significance 
in the regulation of the general blood-pressure, but is concerned in 
local augmentation of blood-flow in response to local needs as in 
increased glandular or muscular activity. So far as we know there 
is no tonic activity of the vasodilators. How the stimulation of the 
dilator fibers leads to dilatation of the vessels is a subject of specu- 
lation. Howell has contended that it is probably by direct inhibition 
of the muscles in the vessel walls. Vasomotor nerves have been 
shown to exist in all vessels except those of the heart, the lungs, and 
the brain; concerning these three organs the matter is still unsettled. 

Chemical Regulation. — The possibility of a chemical regulation 
of vascular tone has attracted some attention. Gaskell has shown 
that acids in low concentration cause vascular dilatation, and in 
this connection the local action of lactic acid and carbon dioxide 
generated during muscular activity has been suggested. 

The idea that a continued pouring of epinephrin from the adrenal 
glands into the circulation is a factor in the maintenance of normal 
vascular tone is now questioned. Hoskins and McClure 1 have 
obtained no fall in blood-pressure after ligation of the adrenal vessels. 
They have also found that an amount of epinephrin in the circulation 
sufficient to affect the blood-pressure is enough to cause suppression 
of intestinal peristalsis. The various studies tending to show by 
one test or another that there is adrenalin demonstrable in the 
circulating blood have been shown by Stewart, O'Connor, Schultz, 
and Janeway and Park to be based on unreliable methods, and 
as Janeway and Park 2 assert, at the present time there is no evidence 
that epinephrin, in amounts sufficient to produce its physiological 
effects upon any hitherto used test objects, exists in the circulating 
blood, with the exception of the blood from the suprarenal vein. 
Cannon's 3 recent work, indicating that after excitement in cats 
there is an increased output of adrenal secretion, suggests that this 
may be a factor in the rise of general arterial pressure incident to 
excitement or exertion. As to the action of other organs of internal 
secretion upon the maintenance or regulation of blood-pressure 
the findings are inconclusive. Extracts of the pituitary gland 
produce on injection a brief fall in blood-pressure, followed by a 
rise. The depressor substance is related to cholin. 4 The pressor 

1 Amer. Jour. Physiol., 1911-12, xxx, 192; ibid., 1912-13, xxxi, 59. 

2 Jour. Exper. Med., Lancaster, 1912, xvi, 541. 

3 Amer. Jour. Physiol., 1913, xxxii, 44. 

4 C. J. Wiggers, Amer. Jour. Med. Sci., 1911, cxli, 502. 
3 



34 THE PHYSIOLOGY OF BLOOD-PRESSURE 

substance differs somewhat in its effects from that obtained from 
the adrenals. Extracts of various mammalian tissues, thyroid, liver, 
pancreas, thymus, testis, bone-marrow, the intestine from various 
levels, parathyroid, brain, prostate, ovary, in the hands of most 
observers produce on injection a fall of blood-pressure. 1 ' This fall 
may be due in some instances to the presence of cholin. A pressor 
substance has been obtained from the kidney, and certain observers 
with some of the above-mentioned organs from certain mammals 
have obtained pressor instead of, or in addition to, depressor effects. 
This action of tissue extracts from such diverse sources is not, 
however, to be understood to mean that these organs are during 
life pouring into the blood-stream substances serving to influence 
and regulate blood-pressure. We have no proof that the substances 
extracted from these organs ever pass normally from them into the 
blood-stream, nor that they have anything to do with the regulation 
of blood-pressure. 

The Blood and the Lymph. — Within a wide range the tonus of the 
capillaries and veins compensates for changes in the total volume 
of blood. Thus, 2.8 per cent, of the body's weight, or about one- 
third of the entire volume of an animal's blood, may be withdrawn 
without any fall in the arterial pressure. Upon the withdrawal of 
a somewhat larger quantity, however, the capillaries and veins no 
longer can maintain an adequate supply to the right auricle. Dim- 
inution in the cardiac output results and the arterial pressure falls. 

The effect on blood-pressure of the infusion of normal saline 
intravenously depends upon whether the pressure is normal or low 
at the time of the introduction. If the pressure be normal, Cohnheim 
showed that large quantities of normal saline may be introduced 
intravenously with only very slight and transitory elevation of 
blood-pressure. This is because the fluid introduced is rapidly 
removed by the kidneys and intestines. When, however, the blood- 
pressure is much below normal, either as the result of loss of vaso- 
motor tone or of hemorrhage, the effect of introduction of normal 
saline is considerable and is persistent. The injection of defibrinated 
blood, however, as Mall has shown, always produces a marked 
rise of blood-pressure. It is possible by this means to raise and 
maintain the aortic pressure very considerably above normal. 
This is probably due to the content of colloidal substances in the 
blood which cannot be removed by kidney or intestine and which, 

' J. M. Miller and E. M. Miller, Jour. Physiol., 1911, xliii, 242. 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 35 

being retained, retain the fluid also. Knowlton 1 has shown that 
intravenous injection of colloidal solutions, such as gelatin, causes 
a similar persistent rise of blood-pressure without diuresis. 

That the lymphatic system to some extent acts as a regulator of 
the amount of blood is unquestionable. Its action, however, is 
not very rapid and is limited in extent. It has been demonstrated 
that a rise in arterial blood-pressure is associated with increase in 
the proportion of erythrocytes, leukocytes, and dry substance of 
the blood, while a fall in arterial blood-pressure results in decrease 
in the proportion of these elements. This is probably largely to be 
explained by passage of the fluid elements of the blood into the 
lymphatic channels or vice versa — a transfer which has been supposed 
to take place chiefly in the lungs. 

Viscosity of the Blood. — Increase in the viscosity of the blood 
increases the resistance to its passage through the vessels and in 
consequence tends to the elevation of blood-pressure, and vice versa. 
Clinically, thus far, no definite relationship has been established 
between the degree of hemic viscosity and the height of blood- 
pressure. 

Blood-pressure and Blood-flow. — The purpose of blood-pressure is 
the maintenance of blood-flow. The rate of blood-flow between 
two points is determined solely by the difference of blood-pressure 
between these points and by the resistance to be overcome in the 
connecting vessels. An increased difference of blood-pressure 
between two points with the same resistance must result in an 
increased blood-flow from the one to the other. Unaltered difference 
of blood-pressure between two points with diminished resistance 
will likewise result in an increased blood-flow from the one to the 
other. Increase in the physiological activity of any organ of the 
body demands an increased blood-flow through the organ. Prac- 
tically all physiological changes in the resistance in the arterioles 
and capillaries, and in the arterial blood-pressure, are to be looked 
upon as the normal mechanism for securing the proper distribution 
of blood to the various organs and tissues of the body. 

It is not to be supposed, however, that blood-flow is proportional 
to blood-pressure alone. Indeed, abnormally high blood-pressure 
is associated frequently, perhaps usually, with a diminished blood- 
flow due to an abnormal degree of resistance in the peripheral 
vessels. Nor is high blood-pressure to be considered an indication 

1 Jour. Physiol., 1911, xliii, 219. 



36 



THE PHYSIOLOGY OF BLOOD-PRESSURE 



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BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 37 

of normal cardiac power, since all the reserve power of the cardiac 
muscle may have been exhausted in maintaining this very pressure, 
and the heart may be at the point of failure with beginning dilatation 
and yet the pressure may still be maintained above normal. 

These relations between blood-pressure and blood-flow are indi- 
cated somewhat crudely in the accompanying table of the typical 
effects of various procedures upon blood-pressure and upon blood- 
flow, both total and in certain vascular areas. It will be noted that 
there are conditions which alter the blood-flow through the skin 
and extremities in an opposite sense from that of the total blood-flow. 
This fact must be kept clearly in mind in employing those methods 
in clinical use for estimating blood-flow through the hand and arm. 

Systolic, Diastolic, and Pulse Pressure. — In the discussion so far 
we have considered chiefly the effects of various factors upon mean 
blood-pressure and the relation of mean blood-pressure to blood-flow. 
Inasmuch, however, as in clinical work it is not the mean pressure 
but the systolic and diastolic pressure that we measure, the relation 
of these to the mean pressure under various circumstances must be 
considered. As already stated, there is no constant numerical 
relation between these three phases of blood-pressure that makes 
it possible from any two to calculate the third. It may be affirmed, 
however, that the mean pressure follows more closely in its fluctua- 
tions the diastolic pressure than it does the systolic, and the study 
of the diastolic pressure is therefore in many ways of greater value 
than is that of the systolic. Dawson's 1 rule for roughly estimating 
the mean -pressure in man is to add one-third of the pulse pressure 
to the diastolic pressure. The effect of various procedures upon 
these phases of blood-pressure, upon cardiac rate and upon blood- 
flow through various vascular areas, is shown in the accompanying 
table. It will be noted that the systolic, diastolic and mean pressures 
are altered in the same direction by most procedures — not, however, 
always to the same extent. Under some circumstances, notably 
in aortic regurgitation, this, as will be seen from the table, is not 
the case. In the average normal individual at rest the diastolic 
is 70 per cent, of the systolic pressure, but in not a few normal 
cases it may be as high as 85 per cent. 

Pulse Pressure. — The pulse pressure is with qualifications an 
indication of the cardiac output per beat. As a rule increased 
ventricular output leads to increased pulse pressure and vice versa. 

1 Loc. cit. 



38 THE PHYSIOLOGY OF BLOOD-PRESSURE 

The pulse pressure normally ranges between 35 and 50 mm. Hg. 
With very few exceptions it should not fall below 20 per cent, of 
the diastolic pressure. The attempt has been made to establish 
formulas enabling one from the pulse pressure and the cardiac rate 
to estimate alterations in the cardiac output per minute — in other 
words, of the blood-flow from the heart. The accompanying table 
shows that, as a rule, changes in pulse pressure and aortic flow are 
in the same direction, but that this is not always true, for aortic 
regurgitation and so common a condition as arteriosclerosis tend 
to- produce alterations of these factors in contrary directions. 
Moreover, only under very limited conditions is there any constant 
quantitative relation between the respective changes in these fac- 
tors. Hence all attempts aiming to express in figures the blood- 
flow on the basis of the pulse pressure should be regarded with 
suspicion. 

Effects of Respiration on Blood-pressure. — Ludwig, 1 in 1847, first 
showed that respiration affects the aortic pressure. The following 
analysis of these effects is from Tigerstedt. 2 

When the vagi are cut and the lungs are being artificially ven- 
tilated, the capillaries of the lungs are compressed as the lungs are 
inflated, and dilated as the lungs are emptied. The first effect of 
inflation is therefore to drive the blood from the pulmonary capil- 
laries on into the left ventricle (A) with increased output and rise 
of aortic pressure. The capillary constriction then acts as a dam to 
further transmission of blood, the inflow to the left ventricle dimin- 
ishes and aortic pressure falls (B). This is still more marked when 
the lungs are first deflated and the capacity of the pulmonary 
capillaries is increased (C). Once they become filled, however, 
they readily transmit a liberal supply to the left heart and the 
aortic pressure rises (D), to be still further increased as inflation 
again begins (A). If respiratory movement be made very rapid, 
the phases B and D are eliminated and the highest pressure comes 
at the end of inspiration, the lowest at the end of expiration 
(Fig. 7). 

In natural respiration the relations are altered. During inspira- 
tion the pulmonary capillaries are first distended and while filling 
with blood retard its onflow (A), but when dilated permit a ready 
flow through to the left heart (B) ; with the beginning of expiration 
they are compressed, emptied into the left heart with elevation of 

1 Arch. f. Anat. u. Physiol., 1847, vi, 242. 

2 Lehrbuch des Kreislaufes, 1893. 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 39 

the aortic pressure (C), but during the remainder of expiration they 
offer considerable resistance to the onflow of the blood ( D) (Fig. 8). 
Erlanger and Festerling 1 find the phases A and C so long as to 
almost do away with phases B and D. They note toward the end 
of inspiration an acceleration of cardiac rate which tends to increase 
aortic pressure, and toward the end of expiration a retarding of 
cardiac rate. 




These changes in cardiac rates, first noted by Ludwig, do not 
occur if the vagi have been cut; they are therefore reflex phenomena. 
Einhodt, Talma, Kronecker and Heinricius believe the aspiration 
of blood into the thorax during natural inspiration tends to increase 
diastolic filling, and diminish systolic emptying with a lowering of 
blood-pressure and, vice versa, in expiration. Fredericq has shown 
that if in an animal with artificial respiration and cut vagi and 
phrenics the artificial respiration be suspended, respiratory move- 
ments of the thoracic wall occur. These are, of course, without 
effect either on the pulmonary blood-flow or ventilation. How- 
ever, during the inspiratory movement a fall of aortic pressure 



AORTIC 
BLOOD 
PRESSURE l\ A 




INSPIRATION EXPIRATION INSPIRATION EXPIRATION 

Fig. 8 



occurs; during the expiratory movement, a rise. These changes 
can only be explained as effects arising from the vasomotor centre 
which induce alterations in peripheral resistance. There is there- 
fore a coordination between the three centres, the respiratory, 
cardio-inhibitory and vasomotor as follows : 



Respiratory. Vasoconstrictor. 

Inspiration Inhibition (dilatation) 

Expiration Stimulation (constriction) 



Cardio-inhibitory. 
Cardiac acceleration 
Cardiac retardation 



1 Jour. Exper. Med., 1912, xv, 370. 



40 THE PHYSIOLOGY OF BLOOD-PRESSURE 

Obviously the changes in the cardio-inhibitory and vasomotor 
centres have opposite effects on the blood-pressure. Fredericq's 1 
experiment shows that these changes are not due, as Schiff supposed, 
to changes in the gases of the blood, the result of pulmonary ven- 
tilation. 

The inspiratory fall of the diaphragm raises abdominal pressure, 
and serves as an adjunct to the aspirating action within the thorax 
in sending the blood from the abdomen into the thorax. 

Henderson has concluded from recent experimental studies that 
the variations in arterial pressure are of the same character and bear 
the same relations to the phases of respiration in an animal which 
is breathing spontaneously after the chest has been opened, as in 
a subject with the thorax intact. This would argue against the 
importance of the changes in intrathoracic pressure as an explana- 
tion of the respiratory changes in arterial pressure. He concludes 
that with normal venous pressure, the respiratory variations of 
blood-pressure are always accompanied by and are due to asso- 
ciated changes in pulse rate, accelerated rate causing higher pressure. 
On the other hand, with a deficient venous pressure, such as exists 
frequently under experimental conditions, after hemorrhage or in 
shock, forcible expiratory contractions of the diaphragm may 
increase the venous pressure sufficiently to more than compensate 
for a slower pulse rate during expiration. 

In animals under experimental conditions, the pulse as already 
noted, usually quickens during inspiration and slows during expira- 
tion. In man not only this relation but, according to Putzig, 2 the 
exact opposite and many intermediate synchronisms likewise 
occur. Henderson and Barrington find, however, that in the large 
majority of their studies both from man and animals, no matter 
what the relation of pulse rate to respiratory phase may be, 
arterial pressure rises with the cardiac acceleration and falls with 
retardation. 

Summing up the effects of respiration on the cardiovascular 
system under normal conditions we find: 

Inspiration: First, fall of aortic pressure; second, cardiac accel- 
eration, possibly slight rise of aortic pressure. 

Expiration: First, rise of aortic pressure; second, cardiac retarda- 
tion, possibly slight fall of aortic pressure. 

These fluctuations of pressure, synchronous with respiration, con- 

1 Arch. Ital. de Biologie, 1882, iii, 55. 

2 Ztschr. f. Exper. Path. u. Therap., 1912, xi, 115. 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 41 

stitute the second order of blood-pressure oscillations. In normal 
individuals these waves are a negligible factor in clinical observa- 
tions, but in labored respiration they may amount to S to 10 mm. 

Traube-Herring Waves. — These were first noted by Traube. 1 He 
observed that in a curarized animal with artificial respiration, if 
the respiration was suspended, the aortic pressure rose and remained 
high for two or three minutes and that during that time, without 
any movements of the animal or any respiratory movement, the 
arterial pressure showed slow waves, about seven per minute, that 
might have an amplitude of 40 mm. of mercury. The cardiac rate 
remained unaltered. After two or three minutes the arterial pressure 
began to fall and from this moment these waves ceased, or at most 
a few feeble ones were observed. If, now, artificial respiration were 
resumed, these slow waves, perhaps only two per minute, might again 
for a while be observed, the waves due to the artificial respiration 
and to the cardiac cycles being superimposed upon them. He 
considered these waves the result of the stimulus of CO2 upon the 
vasoconstrictor centre, and succeeded in producing them by main- 
taining respiration with an atmosphere containing 20 per cent, 
of CO2. The tracing in Fig. 6 illustrates these oscillations. 

Intrapericardial Pressure. — If a cannula be introduced into the peri- 
cardium of an animal, the pericardium ligated around the cannula 
and normal saline introduced in such a way that its pressure may 
be measured and controlled, it will be found that a very slight 
positive intrapericardial pressure will cause a fall of aortic blood- 
pressure with a diminished cardiac output. When the pressure 
rises to even so low a figure as 8 to 10 mm. Hg. the cardiac output 
becomes practically nil and there is a rapid extreme fall of aortic 
blood-pressure. This phenomenon is due undoubtedly to occlusion 
of the great veins supplying the auricles, by an intrapericardial 
pressure exceeding the venous pressure. 

Intra-abdominal Pressure. — If, while recording the carotid or 
femoral pressure of a dog, pressure be exerted over the abdomen 
with the hand or in any other way, the arterial blood-pressure will 
be seen to rise 10 to 20 mm. Hg. and to remain at a somewhat 
elevated level while the pressure is maintained. This is due to 
the fact that, as already noted, the splanchnic vessels constitute 
the great reservoir for the blood. Increase of intra-abdominal 
pressure tends to empty these vessels onward into the right auricle, 

1 Cent. f. d. med. Wiss., 18G5, iii, 881. 



42 THE PHYSIOLOGY OF BLOOD-PRESSURE 

and hence by increasing the venous supply to the heart to increase 
the cardiac output. At the same time the additional pressure 
increases somewhat the resistance offered to flow through the 
mesenteric capillaries, and hence resistance of the most important 
vascular area from the stand-point of the determination of blood- 
pressure. By both means increased intra-abdominal blood-pressure 
leads to increased arterial blood-pressure. Conversely, relaxation 
of the abdominal walls favors low arterial blood-pressure with 
stasis of the blood in the splanchnic area, but this tendency may 
be entirely counterbalanced by adequate vasomotor tone in these 
vessels. 

Burton-Opitz 1 has shown that an increased intra-abdominal 
pressure up to 20 to 30 mm. Hg. causes an increased blood-flow 
and blood-pressure in the carotid arteries and external jugular 
veins and also an increased blood-pressure in the femoral artery. 
There is evidently brought about, therefore, a shifting of the blood 
from the splanchnic to the peripheral circulation and especially 
to the head under such conditions. 

Extremely high intra-abdominal pressure, as from a very large 
ascites, may interfere with the return of blood to the heart, and 
lower arterial blood-pressure. 

Blood-pressure and Intracranial Pressure. — The brain is enclosed 
in a bony encasement and is, so to speak, floating in the cerebro- 
spinal fluid. This fluid fills the subarachnoid space, the ventricles 
and their communicating passages; all these spaces are normally 
in free communication. 

Evidence indicates that the pressure of the cerebrospinal fluid 
is always equal to the venous pressure in the brain sinuses. This 
pressure may vary from in the upright position (Hill) 2 to 50 or 
60 mm. Hg. in the convulsions of strychnine poisoning, or even 
more in cases of brain tumor. If the intracranial pressure exceeds 
the carotid pressure the circulation through the brain becomes 
entirely checked, due to compression of the capillaries. Complete 
occlusion of the larger cerebral arteries occurs, however, only when 
the intracranial pressure is raised (experimentally) to about 150 
mm. Hg. above the carotid pressure (Eyster, Burrows and Essick). 3 
The cerebral anemia produced by a rise of intracranial pressure 

1 The Carotid Blood Flow in Relation to the Intra-abdominal Pressure, Amer- 
Jour. Physiol., 1914, xxxvi, 64. 

2 The Physiology and Pathology of the Cerebral Circulation, London, 1S96; Proc. 
Royal Soc, 1894, lv, 52. 

3 Jour. Exper. Med., 1909, xi, 489. 






BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 43 

to the level of the carotid pressure was shown by Cushing 1 to produce 
two reflex effects: (1) stimulation of the vagus with slowing of 
the cardiac action; (2) stimulation of the vasomotor centre, with 
general vasoconstriction and rise of carotid pressure to the level 
of the intracranial pressure, and in consequence the reestablishment 
of the cerebral circulation. If the increase of intracranial pressure 
be very gradual the vagus excitation may not be elicited. Cushing 
likewise studied the effects of localized pressure upon portions of 
the brain and obtained various results dependent upon the location 
selected. Pressure upon the medullary centres acts as does increase 
in general intracranial tension. The elevated blood-pressure asso- 
ciated with intracranial pressure secondary to neoplasms of the 
brain is to be considered a compensatory and beneficent process 
for the maintenance of blood-flow through the vital centres. If this 
compensatory rise does not occur, absolute cerebral anemia results. 
The time that different portions of the brain can endure anemia 
and recover varies greatly. Experiments by Crile and Dolley 
showed that the central nervous system of young animals endures 
anemia better than that of older ones. These parts of the brain, 
which preside over conscious life, the higher psychic centres, were 
in no instances resuscitated after total anemia of eight minutes, 
but always after only four minutes. The vasomotor centre was 
frequently resuscitated after fifteen minutes, occasionally after 
eighteen, once after twenty, -and once in a puppy after thirty 
minutes. The respiratory centre was more resistant, moderate 
reaction being obtained after as much as forty minutes of total 
anemia. We may say, therefore, that reduction of arterial pressure 
results in lessened blood supply and, as a rule, diminished activity 
within the brain; that if this reduction be great enough, complete 
anemia of the brain results with cessation of its activities, and 
unless the blood-supply be promptly restored, a permanent cessa- 
tion ; also that the arterial blood-pressure, so far as it concerns the 
brain, must be considered with relation not to the atmospheric, 
but to the intracranial pressure, hence a rise of intracranial pressure 
is equivalent to a fall of blood-pressure, and vice versa. 

Blood-pressure and Intra-ocular Pressure. — The chambers of the 
eyeball are filled with fluids which distend the eyeball and maintain 
a pressure in these cavities normally of about 20 to 30 mm. Hg. in 
man. The intra-ocular pressure is measured by one of two methods : 

1 Mitteil. aus den Grenz. der Med. u. Chir., 1902, ix, 791; Amer. Jour. Med. Sci., 
1903, cxxv, 1017. 



44 THE PHYSIOLOGY OF BLOOD-PRESSURE 

(1) Ophthalmomanometry, in which the pressure is measured 
directly by introducing a hollow needle into one of the chambers, 
preferably the anterior, and connecting it with a suitable manometer 
or system of manometers; (2) ophthalmotonometry, in which the 
degree of internal pressure is estimated by the amount of resistance 
to deformation offered by the walls of the eyeball. Obviously 
only the second method is, as a rule, applicable to man; it has, how- 
ever, certain fallacies and objections among which are the error 
introduced by the inherent rigidity of the ocular walls, that due to 
the increase of intra-ocular pressure caused by the distortion of the 
eyeball, as well as the dangers and discomforts of the application of 
the instrument. These errors in the latest instruments are, however, 
largely eliminated. The pressures in the aqueous and vitreous 
chambers of the eye are practically identical, not differing by more 
than 1 mm. Hg. The distensibility of the walls of the eyeball is 
so slight that under ordinary conditions any increase in the fluids 
within the eyeball, either in one of the chambers or in vessels of 
the choroid, must cause an increase in the intra-ocular pressure. 
This fact leads to almost complete suppression of the visible pulsa- 
tion of the retinal arteries. Likewise the pressure in the blood- 
vessels, including capillaries and veins, can never fall below the 
intra-ocular pressure without collapse of these vessels and cessation 
of the flow through them. Since the outflow from the veins of 
the eye is usually a steady stream the venous pressure must be 
normally equal to the intra-ocular pressure. The capillary pressure 
within the eye is supposed by Parsons 1 to be 40 to 50 mm. Hg., 
and that in the veins to equal the intra-ocular pressure. 

The fluids distending the eyeball circulate along one of two 
courses: (1) That of the blood entering the ciliary arteries and 
leaving by the scleral veins, the venae vorticosse; (2) that of the 
lymph fluids filling the vitreous and aqueous chambers, entering 
the vitreous chamber from the vessels of the ciliary processes, passing 
into the aqueous chamber and leaving at the filtration angle by 
the spaces of Fontana for the canal of Schlemm and thence into 
the scleral veins. As long as the intra-ocular tension is to remain 
constant the combined inflow along these two courses must equal 
the combined outflow. All evidence indicates that the rate of 
secretion of lymph into the posterior chamber is proportional to 
intracapillary pressure in the eyeball. Therefore an increase of 

1 Diseases of the Eye, Philadelphia, 1912. 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 45 

intracapillary pressure not only tends to increase Lntra-ocular 

tension directly, but also indirectly by increasing lymph production. 
Rapid changes in intra-ocular pressure are probably due, as a rule, 
to changes in intravascular pressure and volume; slower changes 
may be due to alterations in the rate of lymph formation or removal. 
It is possible, as shown by ophthalmoscopic examination, to have 
distention of the retinal arteries and veins with normal intra- 
ocular tension due to compensatory adjustment in the quantity 
of lymph. As a rule, however, the intra-ocular pressure is closely 
related to the circulatory conditions in the eyeball. 

The Intra-ocular Pressure Rises. — 1. With increase in the arterial 
pressure in the arteries supplying the eyes, as from compression of 
the thoracic aorta, stimulation of the vasomotor centre or of the 
splanchnic nerves, asphyxia, general effects of adrenalin, injection 
of normal saline, etc. At times the intra-ocular tension may be 
shown to vary with the respiratory or the Traube-Herring blood- 
pressure waves. 

2. With local dilatation of the arterioles of the eyes. The exist- 
ence of vasomotor fibers for these vessels has not as yet been satis- 
factorily demonstrated, since changes in the intra-ocular pressure 
following stimulation or section of various nerves may in all cases 
be attributed either to effects upon the general blood-pressure, or 
to stimulation of the extra-ocular muscles (v. infra). 

3. From venous obstruction. Rise in general venous pressure 
is probably never sufficient to counterbalance the contrary effects 
of the associated fall of arterial pressure. Moreover, the relatively 
high venous pressure within the eyeball renders considerable changes 
in general venous pressure of but slight moment. On the other 
hand, local venous obstruction, as by ligation of the venae vorficosse, 
leads to marked rise of intra-ocular pressure (up to 90 mm. Hg.), 
(Adamuk, Leber, Koster, Gzn) with increased transudation of 
highly albuminous lymph. There follows a slow return to normal 
pressure in the course of a few weeks. 

4. From increased lymph formation from any of the above- 
named causes of increased capillary pressure. 

5. From decreased lymph drainage either from venous obstruc- 
tion or from obstruction of the filtration angle, as with pupillary 
dilatation in glaucoma. 

The intra-ocular tension falls as the result of the reverse of the 
above-mentioned factors : 

1 . From fall in the blood-pressure in the arteries supplying the eyes. 



46 THE PHYSIOLOGY OF BLOOD-PRESSURE 

2. From local arteriolar constriction such as may be obtained 
from adrenalin (Parsons) or nicotin (Henderson and Starling) 
by injection into the carotid, their local effects preceding their 
general systemic effects. 

3. From diminished lymph formation secondary to any of the 
above-named causes of reduced blood-pressure. 

4. From improved lymph drainage, as by freeing of the filtration 
angle by pupillary contraction. 

The Relation of Blood-pressure to Secretion. — The activity of all 
glands is associated with increased blood-flow through the gland. 
This increased blood-flow that is associated with glandular activity 
was early noted in connection with chorda tympani stimulation 
and the resultant abundant flow of saliva. It was naturally sug- 
gested that the abundant flow of saliva might be entirely the result 
of the increased circulation and capillary blood-pressure in the 
gland, due to the vasodilator fibers in the chorda tympani. Ludwig 1 
showed, however, by measuring the pressure in the salivary duct 
by means of a manometer that following stimulation of the chorda 
tympani the pressure in the salivary duct might exceed the blood- 
pressure. Moreover, if blood-pressure be shut off from the gland, 
stimulation of the chorda still gives secretion for a short time, 
whereas if atropin be injected into the gland, chorda stimulation 
causes dilatation of the vessels and increased blood-flow but no 
secretion. Hydrochlorate of quinine injected into the gland causes 
vascular dilatation but no secretion. Therefore, while an abundant 
blood-flow is essential for the proper functioning of actively secret- 
ing glands, it is not in itself the cause of the increased secretion. 

Effects of Exercise on Blood-pressure. — The effect of exercise on 
blood-pressure has been studied by many. One of the first inves- 
tigations was that of Marey 2 who measured the systolic pressure 
in the carotid of a horse before and after a run of ten minutes and 
noted a fall from 108 mm. Hg. before to 102 after. Kaufmann 3 
likewise found after prolonged exertion in horses a fall of pressure. 
Almost uniformly, however, the other observers, investigating for 
the most part the dog and man, have noted a rise in pressure after 
exercise. Tangl and Zunst 4 measured the maximal and minimal 
carotid pressures in the dog and from them calculated the approxi- 
mate mean pressure. After having the animal run up steps they 

1 L. Hill and M. Flack, Proc. Royal Soc, London, 1912, S. B. lxxxv, 312. 

2 Traveaux du Laboratoire, 1876. 3 Arch. f. d. ges. Physiol., 1892, liii. 
4 Ibid., 1898, lxx, 544. 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 47 

found a rise of from 6 to 23 mm. Hg. After very severe exertion 
the elevation was extreme, amounting to 120 mm. Hg. Experiment- 
ing upon himself, von Basch 1 had, in 1887, noted after a quick ten- 
minute climb up a hill a rise from 125 mm. Hg. to 180 mm. Von 
Maximowisch and Rieder 2 studied the effect on 27 individuals of 
2500 kg. of work performed on a Gartner ergostat in three to 
five minutes and they obtained in 21 individuals a rise; in 5, no 
change; and in 1, a fall of systolic pressure; the greatest rise was 
50 mm. Hg.; the one fall was 20 mm. Oertel 3 in 8 individuals 
after mountain climbing noted a rise in all, varying from 3 to 43 
mm., the average being 17 mm. A rise after exertion has likewise 
been noted by Zadek, 4 Friedmann, Grebener 5 and Griinbaun, 6 Edge- 
comb and Bain, Eichberg, 7 Russell, Williamson, 8 Routhier and 
Boussaguet, 9 and Graupner. 10 Moritz 11 obtained somewhat similar 
results. Bruck 12 has noted in man with the Riva-Rocci and 
with the Hurthle apparatus an immediate rise upon commenc- 
ing sudden severe exertion, up to 30 or 40 mm. Hg., followed 
after a few pulse beats by a fall to subnormal and then a prompt 
return to from 18 to 38 mm. above normal. This brief primary 
rise he attributes to increased intrathoracic pressure. He measured 
the intrathoracic pressure by introducing a rubber bag into the 
esophagus and found it at the time of the primary rise of blood- 
pressure to be from 50 to 130 mm. Hg. This pressure forces the 
thoracic blood on into the left ventricle and hence into the aorta 
with rise of pressure. The following brief fall he attributes to 
interference with the entrance of more blood into the thorax. 

Erlanger and Hooker, 13 making graphic records of maximal and 
minimal pressure in man, find that very moderate muscular exer- 
tion as, for example, walking, may diminish the minimal pressure 
while increasing the pulse pressure, pulse rate, and presumably the 
blood-flow. More severe muscular exertion increases these and in 
addition the minimal pressure. 

Probably the chief cause of the increased pressure accompany- 
ing exercise is increased cardiac activity. A factor in influencing 

1 Berl. klin. Woch., 1887, xxiv, 206. 2 Deutsch. Arch. f. klin. Med., 1890, xlvi. 
8 Therapie d. kreislaufstoriingen, v. Ziemssen's Handbuch d. allg. Therapie, iv. 
4 Zeitsch. f. klin. Med., 1881, ii, 509. > Wien. med. Jahrbuch., 1882, p. 197. 
6 Wien. med. Presse, 1899, xl, 49. 7 Jour. Amer. Med. Assoc, 1908, li, 1000. 

8 British Med. Jour., 1909, i, 530. 

9 Compte rend, de la Soc. de Biol., Paris, 1910, lxviii, 1037. 

10 Deutsch. med. Woch., 1906, xxxii, 1028. 

11 Deutsch. Arch. f. klin. Med., 1903, lxxvii, 339. 

12 Ibid., 1907, xci, 171. 

13 Johns Hopkins Hospital Reports, 1904, xii, 53. 



48 THE PHYSIOLOGY OF BLOOD-PRESSURE 

greatly the rise of pressure accompanying exertion is the degree 
of mental effort involved. An unusual form of exertion or one 
requiring close attention causes much more increase of pressure 
than the same amount of work performed in the course of habitual 
action. Thus, Karrenstein 1 found in 172 observations on 72 soldiers 
making a 5.7 km. march in seventy minutes, that 39.5 per cent 
showed a rise, 16.3 per cent, no change, and 44.2 per cent, a fall; 
the average pressure before and after the march was unchanged. 
Of 39 observations on 25 soldiers following a two to three hours' 
march, 12.8 per cent, showed a rise and 69.2 per cent, a fall, the 
average being lowered from 106.1 to 98.8 mm. Hg. In these cases 
little if any mental effort was involved. The effect of mental 
effort has been shown by Putermann, 2 who studied with the Gartner 
tonometer the blood-pressure of 43 boys immediately before and 
after a school examination. A rise occurred immediately before 
the examination in 37, a fall in 4. The rise was usually 10 to 20 
mm. Hg., but one rise of 50 mm. was noted. Any excitement may 
lead to a similar rise; indeed, the mere taking of the blood-pressure 
in a susceptible subject. This psychic rise affects the systolic 
pressure more than the diastolic. The acceleration of the pulse 
during exercise is due to depression of the cardio-inhibitory centre. 
It seems that the secondary fall of pressure due to peripheral vaso- 
dilatation is the result of depression of the vasoconstrictor centre 
and not of active vasodilatation, and that a similar depression of 
the respiratory centre may occur from cortical inhibition. 3 

Effects of Posture. — It has already been noted that the chief 
reservoir for the blood is the splanchnic area which of itself can 
contain all the blood of the body. Normally, an adequate return 
of blood from this reservoir to the right auricle is secured by means 
of the vasomotor tone of the splanchnic vessels. In the upright 
posture this return must occur against the force of gravity. In 
the recumbent posture, the antagonistic action of gravity is removed. 
Normally in man the reflex regulation of the splanchnic vasomotor 
tone is such that change from the recumbent to the upright posture 
is immediately compensated by an increased splanchnic vasomotor 
tone, and the aortic blood-pressure is maintained almost unaltered 
or there may be noted even a considerable rise of the diastolic 
pressure. In subjects with defective vasomotor compensation, 

1 Ztschr. f. klin. Med., Berlin, 1903, 1, 322 (bibliography). 

2 Wien. med. Woch., 1904, liv, 265. 

3 Martin and Gruber, The Influence of Muscular Exercise on the Activity of Bulbar 
Centres, Amer. Jour. Physiol., 1913, xxxii, 315. 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 49 

however, there may occur a fall of the aortic blood-pressure upon 
transition from the recumbent to the upright posture, and this may 
be of some diagnostic value. The common treatment of syncope 
by placing the patient recumbent has for its basis the effort to make 
gravity assist instead of resist the action of the splanchnic vaso- 
motor tone, which in this condition as in surgical shock and collapse, 
is inadequate. Change from sitting posture to standing causes, 
normally, according to most observers, a rise of from 5 to 15 mm. 
Hg. of systolic brachial pressure. Erlanger and Hooker, studying 
the minimal and pulse pressures, found usually but not constantly 
on assuming the standing posture a rise in the minimal pressure, 
but a slight fall in pulse pressure. Karrenstein 1 noted a little lower 
brachial systolic pressure in recumbent than in sitting posture. 
On stooping he found in 90.8 per cent, of 153 cases a rise of from 
1 to 45 mm. (average 10.8). The effect of posture upon vessels 
not at the level of the heart has been considered (p. 23). Barach 
and Marks 2 upon changing the posture from the upright to the 
recumbent in an entirely passive manner in forty-eight subjects 
between fifteen and thirty years of age, have observed the following 
effects which differ from those of earlier observers: In changing 
from the erect to the horizontal the maximal pressure was usually 
increased, the cases varying from an increase of 28 mm. Hg. to a 
decrease of 20 mm. Hg. The minimal pressure was almost always 
diminished, varying from an increase of 4 mm. Hg. to a decrease 
of 44 mm. Hg. When the erect posture is resumed after five min- 
utes, the maximal pressure almost invariably falls and the minimal 
almost invariably rises. In the falling of the maximal pressure 
when the erect posture is resumed, it will nearly always fall con- 
siderably below the previous height of the first reading, while the 
minimal pressure may be higher or lower than the first reading 
with almost equal frequency. The pulse pressure in its variations 
follows closely the maximal pressure. Persons with poor muscular 
development show a tendency to reversal of the pressure curve. 

Effect of Feeding. — After eating a full meal Karrenstein 3 noted 
usually a rise of systolic pressure of 10 to 20 mm. Erlanger and 
Hooker 4 obtained variable effects upon minimal pressure, but a 
constant increase of pulse pressure. These authors noted a slow 
increase of pulse pressure throughout the day, it being smallest 
in the early morning before rising. They found immersion of the 
body in warm water to increase minimal pressure, pulse pressure 

1 Loc. cit. 2 Arch. Int. Med., 1913, xi, 485. 

3 Loc. cit. • 4 Loc. cit. 

4 



50 THE PHYSIOLOGY OF BLOOD-PRESSURE 

and pulse rate; in cold water to increase minimal pressure, but to 
decrease pulse pressure and rate. Immediately after the ingestion 
of food the systolic pressure rises (about 8 mm. Hg. in healthy 
young adults), then gradually falls until the beginning of the next 
meal. The diastolic pressure is much less and variably affected 
by feeding. Associated we find an increased pulse rate and pulse 
pressure. 1 

Sleep. — Tarchanoff 2 noted a fall of aortic pressure in young 
dogs of 20 to 50 mm. Hg. during the early stages of sleep. Leonard 
Hill, 3 Brush and Fayerweather, 4 Howell and Brooks, and Carroll 5 
have studied the phenomenon in man and note the greatest fall 
one or two hours after commencement of sleep; this may amount 
to 20 mm. Then begins a gradual rise continuing to the maxi- 
mum, usually reached about 5 p.m. the following day. If sleep 
is disturbed the usual drop is less profound. In day sleepers it is 
the day pressure which is lower than the night. The minimal 
blood-pressure is according to Weysse and Lutz very uniform 
throughout the day, but with a tendency to a slight lowering as 
the day progresses. 

Altitude. — The study of the effects of altitude on blood-pressure 
has been approached in two ways: (1) By the study of the blood- 
pressure of individuals remaining for longer or shorter periods at 
various altitudes, and (2) by the use of the pneumatic chamber to 
change the atmospheric pressure. 

The blood-pressure may either be measured as so many mm. of 
Hg. above the surrounding atmospheric pressure, or the absolute 
pressure of the blood may be measured. It may be stated at once 
that changes in atmospheric pressure are associated with approxi- 
mately equal changes of the absolute blood-pressure in the same 
direction. Thus, if at 760 mm. atmospheric pressure (ordinary 
atmospheric pressure at sea level) the absolute systolic blood- 
pressure is 895 mm. (135 mm. above atmospheric pressure), then 
if the atmospheric pressure be reduced to 460 mm. the absolute 
systolic pressure will be reduced to about 595 mm. Since all the 
manometers ordinarily used measure the elevation of the blood- 
pressure above the surrounding atmospheric pressure, it is this 
difference of pressure that is ordinarily discussed. Moreover, it is 
this difference of pressure and not the absolute pressure which is 

1 Weysse, H. W., and Brenton, R. L., Diurnal Variations in Arterial Blood Press- 
ure, Amer. Jour. Physiol., 1915, xxxvii, 330. 

2 Arch. ital. de Biol., 1894, xxi, 318. 3 Lancet, 1898, i, 282. 
'Amer. Jour. Physiol., 1901, v, 199. 

6 Trans. Assn. Amer. Phys., Philadelphia, 1912, xxvii, 8. 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 51 

the measure of the functional activities of the circulatory system. 
It is to be understood, therefore, that whenever pressure is here 
referred to it is the pressure in excess of the surrounding atmospheric 
pressure, that is, the relative blood-pressure, that is meant. 

The first to study the effects of changes of atmospheric pressure 
upon the blood-pressure was Paul Bert. 1 Upon lowering the 
atmospheric pressure he obtained a slight diminution of the relative 
blood-pressure. 

Lazarus and Schirmunski 2 in 1884 studied a man in the pneumatic 
chamber with the following results : 

Atmospheric pressure. Relative systolic blood-pressure. 

Mm. Hg. Mm. Hg. 

760 135 

670 135 

440 132) Subjective 

380 110/ dyspnea. 

460 118 

660 135 

760 130 

Camus 3 with rabbits in a pneumatic chamber reduced the pressure 
from 760 to 200 mm. with, in some animals, little or no fall of the 
relative blood-pressure, but with other rabbits on reaching about 
250 mm. atmospheric pressure the relative blood-pressure showed a 
marked fall. 

Mosso, 4 with a dog in a pneumatic cabinet, with reduction of 
atmospheric pressure to 228 mm. Hg., obtained a slight fall of rela- 
tive blood-pressure. On the other hand, Frankel and Geppert 5 
and also Dietrick with lowered atmospheric pressure obtained a 
slight rise of relative blood-pressure, while G. Liebig 6 obtained a 
rise in 2 men, but in 2 others a fall. 

The approximate relation of atmospheric pressure to altitude 
is shown in the following table from Camus: 7 

Atmospheric pressure. Altitude. Altitude. 

Mm. Hg. Meters. Feet. 

760 

660 1,148 3,760 

560 2,370 7,760 

460 4,022 13,200 

360 5,945 19,470 

260 .. 8,600 28,180 

200 11,000 36,040 

1 La Pressure barometrique, Paris, 1878. 2 Ztschr. f. klin. Med., 1884, vii, 299. 

3 Jour, de physiol. et de pathol. gen., Paris, 1903, v, 643. 

4 Arch. ital. de Biol., 1909, xliii. 

6 Ueber die Wirkungen der verdunntc Luft, Berlin, 1883, p. 65. 

6 Sitzungsberichte d. gesellsch. f. Morphol. u. Physiol., Munich, 1896, xii, 37. 

7 Loc. cit. 



52 THE PHYSIOLOGY OF BLOOD-PRESSURE 

Studies of individuals actually at various altitudes are not 
numerous. 

Schneider and Hedblom 1 studied the effect on a series of individ- 
uals passing from 1700 elevation to 6000 feet and again later from 
6000 to 14,109 feet. In passing from 1700 to 6000 feet they 
observed falls of relative pressure of from 3 to 7 mm. Hg., with 
no changes in the average diastolic pressure. In passing from 6000 
to 14,109 feet they found an average fall of both systolic and 
diastolic pressures of 7 mm. Hg. and an average rise of pulse rate 
of 26 beats per minute. The effect upon the systolic pressure was 
more constant than that upon the diastolic. The effect of the 
altered altitude was most marked immediately following the arrival 
at the new level, and those individuals showed most changes who 
were most affected subjectively by the change of altitude. Small 
changes of elevation were without any effect. 

Staehelin 2 studied blood-pressure during balloon ascensions to 
a height with atmospheric pressure of 690 mm. without noting 
any effect on either systolic or diastolic pressure. Staubli 3 noted 
at St. Moritz (5800 feet) no constant change in the blood-pressure 
of healthy subjects. 

Clough 4 has recently published studies of the effects of a rapid 
descent of 1700 feet in a mine shaft. He found that the rapid change 
in altitude either up or down frequently caused a fall of systolic 
pressure of 5 mm. He detected no significant difference between 
the average blood-pressure of individuals living at the altitude of 
5000 feet and those at sea level. 

Gardiner and Hoagland 5 studied individuals living for a year 
at an altitude of 6000 feet and found their relative pressures only 
slightly lower than those observed in individuals of the same age 
at sea level. They studied the systolic pressures of 22 college men 
going by train from a level of 6000 feet to 14,109. The average 
relative pressure at 6000 feet was 126 mm. Hg.; on arrival at 14,109 
feet, 121 mm. Hg.; three and a half hours after arrival, 118 mm. Hg. 
Smith 6 in a recent study has concluded that an altitude of 6230 
feet does not produce any consistent alteration of blood-pressure 
in either normal or tuberculous individuals. 

1 Amer. Jour. Physiol., 1908-9, xxiii, 90 (bibliography). 

2 Med. Klin., 1909, v, 361. 

3 Verhandl. d. Kong. f. inn. Med., 1910, p. 695. 
* Arch. Int. Med., 1913, xi, 590. 

5 Trans. Amer. Climat. Assn., 1905. 

6 Effect of Altitude on Blood-pressure, Jour. Amer. Med. Assn., 1915, lxiv, 1S12. 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 53 

Age. — In children the blood-pressure has been declared by 
Michael 1 to be more closely proportional to the height or weight 
than to the age of the child. Sex during childhood appears to be 
of no importance. 

Systolic pressure (Michael). 
Weight. Mm. Hg. 

Infancy 75 to 90 

30 to 40 pounds 95 

40 to 50 " 100 

50 to 00 " 107 

60 to 70 " 112 

70 to 80 " 116 

80 to 90 " 122 

90 to 100 " 126 

Judson and Nicholson 2 give the following table of averages at 
different ages based upon a series of 2300 observations made with 
a modified Erlanger method and by the auscultatory method 
reading the diastolic pressure at the beginning of the fourth phase. 

Age. Systolic. Diastolic. 

3 years 91.8 65.6- 

4 " 91.6 64.9 

5 " 91.3 64.4 

6 " 92.6 67.3 

7 " 94.0 66.3 

8 " .*.... 93.6 64.7 

9 " 94.3 71.0 

10 " 99.2 67.1 

11 " 97.1 65.5 

12 " 102.3 65.2 

13 " 103.6 70.5 

14 " 106.1 67.4 

15 " 105.6 67.5 

During adult life the normal systolic blood-pressure may be 
inferred from the following table from Woley: 3 

Systolic blood-pressure. 
Age. High. Low. Average. 

15 to 30 years 141 103 122 

30 to 40 " 143 107 127 

40 to 50 " 146 113 130 

50 to 60 " 149 115 . 132 

60 to 65 " 153 120 138 

Females during adult life average, according to Woley, about 
8 mm. lower in systolic pressure than males of the same age. The 
diastolic ■pressure is normally, at rest, about 70 per cent, of the 
systolic. (See p. 131.) 

'A Study of Blood-pressure in Normal Children, Amer. Jour. Dis. Child., 1911, 
i, 272. 

2 Amer. Jour. Dis. of Child., 1914, viii, 257. 

3 Jour. Amer. Med. Assn., 1910, lv, 121. 



54 THE PHYSIOLOGY OF BLOOD-PRESSURE 

The average minimal pressure in healthy young males of twenty 
years of age was found by Weysse and Lutz to be 85 mm. Hg. with 
a maximal pressure of 120 mm. 

Melvin and Murray, 1 in a series of normal cases using the aus- 
cultatory method and reading the diastolic pressure at the beginning 
of the fourth phase, find the normal diastolic pressure to range 
from 50 to 82 with an average value of 66, or 56 per cent., of the 
systolic. This is much lower, however, than the gradually recog- 
nized figure. 

THE EFFECTS OF ALTERATION OF BLOOD-PRESSURE 
UPON THE ORGANS OF THE BODY. 

I. Effects upon the Heart. — The first effect of a sudden elevation 
of aortic pressure through increase of peripheral resistance is, as 
we have seen (see p. 31), a reflex inhibition of the heart tending 
to reduce the cardiac output and restore the blood-pressure to 
normal. When a permanent increase in the peripheral resistance 
develops, be it the result of continued arteriolar spasm or of arterio- 
lar fibrosis, although the cardiac output per minute may be, and 
probably often is, diminished, the force of the ventricular systole 
is increased to meet the higher aortic pressure and deliver its output 
against this, and if the nutrition of the heart be good there develops 
a cardiac hypertrophy chiefly of the left ventricle. It may readily 
be seen that this phenomenon is a necessary compensatory adjust- 
ment if an adequate blood-flow through the more resistant arterioles 
is to be maintained. It has been further suggested that the hypo- 
thetical substances which, circulating in the blood, have called 
forth the arteriolar spasm may also act as a direct stimulant to 
the cardiac muscle. This, for example, is true of adrenalin. In 
favor of this view is the fact that hypertrophy in hypertension 
cases in man can be observed, as a rule, not only in the left ventricle 
but in all four chambers of the heart; the hypertrophy of the left 
ventricle is usually greater, however, than that of the other cham- 
bers (Senator). 2 It has also been suggested, but less favorably 
received, that the cardiac stimulation is the primary effect of 
these hypertensive substances, the arteriolar spasm and fibrosis 
being secondary. Experimental evidence bearing upon this point 
is difficult to obtain and to interpret, and the question remains 
unsettled. 

1 British Med. Jour., 1914. ii, 500. 

2 Die Erkrankungen der Nieren, Wien, 1902, p. 114. 



EFFECTS OF ALTERATION OF BLOOD-PRESSURE 55 

The final effect upon the heart of maintaining for a prolonged 
period a blood-pressure considerably above normal is cardiac 
exhaustion beginning, as a rule, with dilatation and weakening of 
the left ventricle. Then follow with falling blood-pressure, which 
may still, however, be considerably above the normal, the signs of 
circulatory failure throughout the body: edema, accumulation of 
fluid in the serous cavities, venous congestion, cyanosis, dyspnea, 
edema of the lungs, renal insufficiency, and the disturbances of 
the internal organs resulting from passive congestion. This out- 
come is hastened by coronary sclerosis, which impairs the cardiac 
nutrition. The effect of low blood-pressure upon the heart is, as 
a rule, to call forth a reflex acceleration of cardiac rate and ac- 
tivity. So far as the coronary circulation suffers from the lowered 
blood-pressure a detrimental influence is exerted on the cardiac 
nutrition. 

n. Upon Arteries and Arterioles. — Associated with continued 
high blood-pressure are, in the great majority of cases, certain 
changes in the vessel walls. These consist of fibrous thickening 
of the inner and outer coats of the arteries and arterioles with 
increase of their elastic tissue. The muscular coat shows sometimes 
a thinning, sometimes a thickening, but the latter is due more 
often to increase of the fibrous tissue of the muscular coat than of 
the muscle tissue itself. That these fibrous changes in the vessel 
walls are the direct result of strains or minute tears consequent 
upon the high blood-pressure has been suggested. That they are 
the direct effect of those toxic substances which have produced 
the arteriolar spasm and high blood-pressure is possible. Finally, 
in some cases these arteriosclerotic changes in the vessel walls 
result from the toxins of acute infections or of syphilis and develop 
before any rise of blood-pressure has occurred; once developed, 
however, they increase the resistance to the flow of blood through 
these vessels. The effect of this in leading in turn to a rise of 
arterial blood-pressure and eventually, if the coronaries be not too 
sclerosed, to cardiac hypertrophy, will be discussed later. 

m. Upon Capillary Pressure, Venous Pressure, and the Pulmonary 
Pressure. — On these high arterial pressure has little effect. The 
arterial pressure is confined between the left ventricle on the one 
hand and the "stopcock," the arterioles, on the other hand, and 
marked changes may occur in the arterial pressure with no change 
whatever in the pressure in the capillaries, veins, or pulmonary 
vessels. 



56 THE PHYSIOLOGY OF BLOOD-PRESSURE 

As we have noted, the capillary pressure is dependent more upon 
the venous than upon the arterial pressure. 

IV. Upon the Kidneys. — Goll's experiments, performed under Lud- 
wig, were the first to show conclusively the effect of changes in 
blood-pressure upon the activity of the kidneys. Goll cut the vagi 
of a dog, determined the blood-pressure by means of a cannula intro- 
duced into the carotid, then from the two ureters collected all the 
urine excreted for half an hour. He then stimulated continuously 
with a weak faradic current the peripheral end of one of the cut 
vagi, thereby diminishing the cardiac activity and causing a fall 
of blood-pressure. This procedure was continued for half an hour, 
during which time the urine from the ureters was again collected. 
It was found that the fall in blood-pressure had markedly reduced 
the amount of urine excreted in the half -hour and that it had reduced 
the water of the urine more than it had the solids, so that while 
the actual amount of solids was reduced, the percentage of solids 
and the specific gravity of the urine were increased. 

He then took another dog and similarly recorded the carotid 
pressure and measured the urine excreted from the two ureters 
for half an hour. He then bled the dog freely; a fall in blood- 
pressure resulted and persisted. During the next half-hour, while 
the blood-pressure was low, the urine was again collected and was 
found as in the first experiment to be reduced in amount; again 
the water was more reduced than the solids. The blood which 
had been withdrawn from the animal was defibrinated and at the 
end of the half-hour was reinjected, restoring the animal's blood- 
pressure to about the original level. The urine was now again 
collected for half an hour and was found to have increased in quan- 
tity to about the original level of excretion and the water had 
increased more than the solids, so that while the elimination of 
solids had increased, the percentage of solids and the specific gravity 
were reduced to about normal. 

Later Meyer performed the following experiment: In a rabbit 
he constricted the vena cava above the entrance of the renal veins 
to half its natural diameter. This, he found, led to the excretion 
of a diminished quantity of highly concentrated urine which con- 
tained albumin. 

It will be observed that, although Meyer's experiment increases 
the blood-pressure in the capillaries of the kidney, it diminishes 
the output of urine. The activity of the kidney is not, therefore, 
proportional to the blood-pressure, as Goll's experiment might 



EFFECTS OF ALTERATION OF BLOOD-PRESSURE 57 

suggest, but to the rate of blood-flow through the reual vessels. 
In both Goll's experiments the fall of blood-pressure reduces the 
flow through the renal vessels, and in Goll's second experiment the 
reinjection of the blood with the resultant rise of pressure increases 
the flow through the kidney. In the same way digitalis, which 
increases the amplitude of the cardiac systole and thus augments 
the cardiac output, thereby raising the blood-pressure and thus 
increasing the blood-flow through the organs, is a drug which 
produces diuresis. On the other hand, adrenalin, when injected 
intravenously, increases the arterial blood-pressure much more 
than does digitalis, but does so by constriction of the arterioles 
and therefore reduces the blood-flow through the organs. The 
effect of a large dose of adrenalin upon the excretion of urine is to 
greatly diminish or entirely stop it during the brief period of the 
drug's effectiveness. The comparison of the effects of these two 
drugs on renal activity is a good illustration of the impossibility 
of estimating the effectiveness of the circulation by the arterial 
blood-pressure. 

Nitroglycerin and the nitrites act chiefly by dilating the arterioles 
and thus lowering blood-pressure. Did they influence all arterioles 
equally their effect would be to increase the blood-flow through 
all the organs, with a lowering of blood-pressure. In fact, however, 
they dilate the mesenteric vessels disproportionately. Very small 
doses may lead to increased blood-flow through the kidneys with 
diuresis. However, larger doses dilate the mesenteric arterioles 
so much more than the renal that the blood-flow is diverted through 
the former with a fall of aortic pressure, and the flow through the 
renal vessels diminishes, as does the urinary output. 

We find, therefore: (1) A rise in the general arterial blood- 
pressure caused by increasing the bulk of the blood or by augmenting 
the cardiac output, increases the blood-flow through the kidneys 
and in consequence the renal activity. (2) A change in the general 
arterial blood-pressure (rise or fall), produced in such a way as to 
diminish the blood-flow through the kidneys, diminishes the renal 
activity. 



CHAPTER II. 

THE INSTRUMENTAL ESTIMATION OF 
BLOOD-PRESSURE. 

No one who has had any experience with instruments of precision 
in controlling his tactile impressions, will flatter himself with the 
delusion that he can gauge endovascular tension with anything 
approaching accuracy with the finger. Extremes are easily recog- 
nized but the intervening moiety is a fertile source of error. The 
size of the vessel, the character of the surrounding tissues, the 
volume of the pulse and the state of the arterial wall itself, all 
contribute to one's confusion. The estimate of arterial tension 
has therefore been relegated to the more exact field of sphygmoman- 
ometric measurement, just as has the determination of alterations 
of bodily temperature to the thermometer. 

With the older methods and with most of the early instruments 
only the systolic pressure could be gauged. This is no longer 
sufficient. It is now possible to estimate the diastolic pressure 
with approximate accuracy by a number of different methods. 
The systolic index alone tells but a part, and that but a small part, 
of the whole story. 

A large number of instruments for the estimation of human blood- 
pressure have been devised and modified. This gradual develop- 
ment will not concern us here as the subject is mainly historic in 
its interest and has already been ably described by others. 1 In 
many of the older instruments, either the principle was faulty or 
the technique unsatisfactory, hence we shall consider mainly those 
which are of practical utility today. 

Nearly all of the modern instruments are constructed with an 
elastic cuff or arm band which, when inflated and encircling one 
of the extremities, compresses, and when the pressure is raised 
sufficiently, obliterates the arterial pulse below the cuff. This 

1 Janeway, The Clinical Study of Blood-pressure, New York, 1904, p. 43; Tiger- 
stedt, Lehrbuch d. Physiologie d. Kreislaufes, Leipsic, 1893, p. 321; Ergebniss der 
Physiologie, 1907, vi, 265; Vachide and Lahy, Arch. gen. de Med., 1902, pp. 349, 
480, 602. 



THE CHARACTER OF THE CUFF 59 

point corresponds to the systolic pressure. It indicates the point 
at which the external pressure is just sufficient to overcome the 
internal resistance (hlood-pressure, velocity, the arterial wall, and 
the surrounding soft tissues). The velocity factor is negligible and 
the resistance of the arterial wall and soft tissues normally does 
not exceed 10 to 7 mm. respectively. Hill has shown that the 
obliteration pressure in the femoral artery of the dog is the same 
(within 1 to 2 mm. Hg.) as the systolic pressure taken in the opposite 
femoral with a cannula and the Hiirthle manometer. 

The amount of pressure required is measured by means of either 
(1) a mercury manometer graded in millimeters; (2) an aneroid; 
(3) a metallic spring manometer; or (4) a compressed-air manom- 
eter with an indicator; depending upon the particular instrument 
employed. 




Fig. 9. — Arm in cross-section with Riva-Rocci cuff: R, outer wall of rubber tube; 
R', inner wall of rubber tube; S, screw fastening; D, clamp; C, silk cover; A, 
brachial artery; H, humerus; T, tube leading to manometer. 

The Character of the Cuff. — The compression may be exerted upon 
the vessel in question either by (a) a limb-encircling, distensible 
elastic cuff (applied to a segment of the arm or leg), or (b) by means 
of a solid or a fluid pad overlying the artery; in either case sur- 
rounded by an external inexpansile fabric. Of these the former 
is more satisfactory (see Fig. 9). 

The accompanying figures illustrate the principles involved in the 
application of a cuff to the arm. In Fig. 9 we have a rubber cuff 
completely encircling the arm, but insufficiently inflated to occlude 
the artery. In Fig. 10 the rubber extends only part way around 
the arm, but the pressure is high and the arterial lumen therefore 
completely obliterated. 

The width of the cvff, as was shown by von Recklinghausen, 1 is 

1 Ueber Blutdruckmessung beim Menschen, Arch. f. exper. Path. u. Pharmakol., 
1001, xlvi, 78. 



60 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

of vital importance. If it is too narrow, readings higher than the 
actual endarterial pressure may be obtained. The soft tissues of 
the arm offer considerable resistance to compression, which may, 




Fig. 10. — Arm in cross-section with Hill and Barnard cuff: R, outer wall of rubber 
bag; R', inner wall of rubber bag; S, strap, fastened by buckle; C, leather cuff; 
A, brachial artery; H, humerus; T, tube leading to manometer. 

however, be largely overcome by lengthening the segment included 
in the cuff. The reason for this is shown in (Fig. 11). 



W W 






W W 
Fig. 11 



If a distended artery is partially obliterated by the pressure 
of a single block — as in the case of a narrow cuff — we not only 
have to overcome the internal pressure of the vessel but also the 



THE CHARACTER OF THE CUFF 61 

oblique tension of the wall and surrounding tissues {W-T), and 
as a result too high readings are obtained. With a series of blocks 
exerting a similar pressure to the square inch, only the outer blocks 
(W) will be concerned in overcoming the pull of the artery and 
tissues at W-T, while the intervening ones (S-S) will exert their 
full pressure. 

With a broad cuff an error of +7 to +9 per cent, may be assumed. 
With a narrow cuff the figure may reach +40 per cent., while 
the Gartner finger ring has a margin of error of +19 per cent. 

There was for a time much discussion as to the accuracy of von 
Recklinghausen's contention, caused by the belief that a cuff of 
12 cm. interfered with the progression of the pulse wave and yielded 
subnormal values. But the correctness of his view has now been 
definitely established by experiments (1) on the cadaver with 
artificial circulation (Gumprecht), (2) on animals (Fellner, Rudinger, 
Schelling and others) ; (3) on the living human subject (0. Muller 
and Blauel, Janeway). A narrower cuff may be advantageously 
employed for children (3 inches, 7 cm.). 

The outer covering of the elastic cuff, whether of canvas, leather, 
or cloth, must be of a non-distensible character and the rubber 
tubing connected therewith must be sufficiently inelastic to prevent 
any oscillation or stretching with increased pressure. If these 
facts are overlooked we introduce a new source of error for which 
we should have to allow with each increment of pressure. For 
this reason the outer covering must completely enclose the elastic 
cuff, which must not be allowed to slip out of place while in use. 
With a view to obviating this possibility, some cuffs are constructed 
in which the outer and inner cuffs are made as one piece (Vaquez, 
Uskoff, Oliver, Janeway). 

The elastic cuff must of course be sufficiently thin and flexible 
to add but a negligible increment to the manometrical pressure. 
This desideratum, as shown by Gumprecht, is easily furnished. 

The Location of the Cuff, etc. — The brachial artery is usually 
selected for blood-pressure estimation because of its accessibility, 
and because either in the erect, sitting, or recumbent postures it is 
at about the cardiac level. The presence of a thin shirt or waist 
between the arm and the cuff produces only a negligible error. In 
fact it is much better to have a shirt interposed but evenly dis- 
tributed than to have a tight sleeve or an undershirt rolled up 
into an arm-encircling band above the cuff. In children the thigh 
is often the preferable site, on account of the smallness of the arm. 



62 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

In adults, especially for purposes of comparative study, either 
the thigh or the calf may be chosen. The brachial artery is con- 
sidered the site of choice because "it gives us the systolic lateral 
pressure within the subclavian, since brachial and axillary are 
continuous in direction, and therefore a near approximation to 
systolic lateral pressure in the aorta. This, combined with estima- 
tion of diastolic lateral pressure in the brachial, which is practically 
the same as aortic diastolic pressure, gives the best insight into 
actual variations of systemic blood-pressure" (Janeway). This 
statement has been questioned by some observers since, as was first 
shown by Bing, the pressure in the two brachial arteries of the 
same individual may vary 20 mm. or more. The brachial pressure 
is generally, but by no means invariably , equal to that of the aorta. 

The cuffs furnished with the Tech and the Mercer instruments 
are so constructed that the stethoscope used for the auscultatory 
method is applied at the level of the cuff and not below it, as is 
usually the case. This gives readings on the average 10 mm. 
higher than those obtained in the usual manner and, in the opinion 
of the author, adds an unnecessary increment of error. 

I. PALPATORY METHOD. 

A. Estimation of the Systolic Pressure. — Method of Application 
for Instruments of the Riva-Rocci Type (Fig. 12). — The rubber 
cuff ( D) (which should be 12 cm. in width) is applied so as to 
encircle the arm or leg, secured by a non-distensible canvas 
or leather cuff, and strapped or tied snugly in place (generally 
above the elbow or knee). The tube connecting with the rubber 
cuff is attached to the manometer (M) (the valve C on the latter 
being opened to admit air), and is inflated by means of a syringe 
bulb or pump (P) from the distal side of the manometer. The 
systolic pressure is read by placing the finger on the radial pulse 
and pumping the mercury well above the point at which the pulse 
at the wrist disappears. We then close the valve (C), open the 
second escapement valve (E), and as the mercury falls note the 
point at which the radial pulse again becomes perceptible. .If 
the disappearance of the pulse during gradually increasing pressure 
is chosen as a criterion for the systolic level, instead of its reappear- 
ance after obliteration during a falling manometrical pressure, 
higher values (3 to 10 mm. Hg.) will be obtained. The return of 
the pulse after obliteration is also a much more sudden and well- 



PALPATORY METHOD 



63 



marked phenomenon than the disappearance during an increasing 
pressure, and the exact moment at which it occurs is much easier 
to determine. It is essential, however, that the pressure should 
be allowed to drop slowly and steadily, otherwise the first few 
small beats will not be appreciated. A much more important reason 
lies in the fact that the lower reading is also somewhat nearer the 




Fig. 12. — The Stanton sphygmomanometer. 



actual intra-arterial pressure, because we more or less counter- 
balance the overestimation caused by the resistance of the arterial 
wall and the tissues of the arm. More accurate readings will 
be obtained if the radial artery is palpated with the ball instead 
of the tip of the finger. The latter should rest against the over- 
hanging edge of the radius, thus permitting the application of a 
very uniform pressure (Hirschf elder) (Fig. 13). 



64 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

The reappearance of the pulse below the point of constriction 
may be recognized by other means. Thus, if instead of the palpat- 
ing finger a sphygmograph is attached to the wrist, or if a second 
cuff communicating with some sort of recording device is substituted, 
the return of the pulse can be made manifest. 

B. Estimation of the Diastolic Pressure. — The estimation of the 
diastolic pressure was, until the auscultatory method was discovered 
and generally adopted, a more difficult and uncertain procedure. 
By means of the last-named procedure, however, we are now able 
to make readings which from the stand-point of accuracy and 
celerity compare very favorably with those employed for the 




Ractfus 

Fig. 13. — Position of the finger in palpating the radial artery. 



systolic pressure. The estimation of the diastolic pressure is 
of the greatest importance and for general clinical purposes no 
examination can be considered complete without it. 

The basis for all determinations of the diastolic pressure rests 
on the fact that when the pressure in the brachial cuff is at the 
diastolic level, the greatest oscillation in the caliber of that portion 
of the artery which lies beneath the cuff will occur. If the cuff 
pressure is higher, only the upper portion of the pulse wave will 
pass through; if lower, the artery will not completely collapse. 
Whichever the method of estimation of the minimal pressure 
employed, the end in view is always that of making manifest, in 



PALPATORY METHOD 65 

one way or another, the exact point at which this alternate maximum 
filling and collapse occurs. Thus by: 

1. Palpation (Strassburger). — The radial artery below the cuff 
is palpated between the finger and the radius, while the mano- 
metrical pressure is slowly increased. It will be noted that at a 
certain point, usually quite well marked, the pulsations suddenly 
become throbbing (knocking or bounding, "klopfend"), owing 
to a complete alternate distention and collapse of the artery. This 
phenomenon occurs when the minimum pressure is reached. The 
first bounding pulse is to be chosen as the criterion (often this 
characteristic continues for some time during the rise of pressure). 
The method has been found very accurate when compared to graphic 
registration; the first bounding wave corresponding to the first 
full wave on the tracing (Gallavardin). iUthough this method has 
been highly recommended by Ehret, 1 who palpates the brachial 
artery immediately below the cuff, we cannot commend it; it 
requires long practice, and even one who is skilled in its performance 
is hampered by too much of the personal equation. 

2. Visualization. — With that pressure in the cuff at which the 
greatest arterial fluctuation occurs, the greatest oscillation will 
also be transmitted to the mercurial column. Hence observation 
of the lowermost point of the maximum mercurial oscillation was 
for a long time used as a criterion of the minimum pressure. Owing, 
however, to its great inertia, mercury is with difficulty set in motion 
by the compressed air, but once in motion its oscillation may be 
maintained or even increased by very slight pressure changes. 
Furthermore, many instruments were equipped with a U-shaped 
manometer so that the actual mercurial fluctuation was diminished 
by half. It has been partly as the result of this that so many 
different instruments have been placed on the market, although, 
of course, compactness, portability, and cost have also entered into 
the problem. 

The Stanton instrument owes much of its well-deserved popular- 
ity to the fact that, being of the single tube type and well propor- 
tioned, it yielded large mercurial excursions. 

The maximum oscillation in other forms of apparatus, spring 
manometers (v. Recklinghausen), aneroids (Pachon, Rogers), is 
also used to determine the point of maximum arterial fluctuation. 

1 Ueber eine einfache Bestimmungsmethode des diastolischen Blutdruckes, Munch, 
med. Woch., 1909, No. 12. 



6G THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 



H. THE AUSCULTATORY METHOD. 

In 1905 Korotkow suggested the determination of blood-pressure 
by auscultation. Owing to its simplicity, celerity, and accuracy 
this method has supplanted all others for clinical work. 

If, instead of palpating the artery below the compressing cuff, 
we apply the bowl of a stethoscope and listen, we will hear a 
variety of sounds during the fall of the mercurial column. Five 
distinct phases can generally be made out and quite clearly 
differentiated : 

(1) A sound not unlike the first cardiac sound. (2) This same 
sound plus a hissing murmur. (3) The murmur disappears and 
only the sound is heard. (4) The sound suddenly becomes very 
much muffled. (5) The sound disappears. These phases occur 
while the pressure in the cuff is falling in the order given. 

The first sound or phase is due to the sudden distention of the 
collapsed brachial artery caused by the return of the pulse wave, 
the sound waves being reenforced by the resonating quality of 
the cuff. (Compression with an Esmarch bandage usually fails 
to produce a sound. Gittings. 1 ) The onset of this phase indicates 
the systolic -pressure. 

The Second Phase. — The addition of a murmur to the first sound 
is due to the formation of fluid veins, whirls, eddies, produced as 
the blood flows past the constriction into the relatively dilated 
artery below the cuff. 

The Third Phase. — Disappearance of the murmur is caused by 
sudden vibrations of the vascular wall produced by the increased 
volume of blood which, although diminished in rapidity of flow, 
now reaches the artery at the point of auscultation. The con- 
stricting pressure being diminished, the fluid veins below the cuff 
gradually disappear. This phase is generally distinctly louder 
than the first. It corresponds to the stage of large oscillation in 
the graphic method, and its end occurs simultaneously with the 
Ehret phenomenon and the last of the maximal graphic waves 
(see Fig. 17). 

The fourth phase 2 — muffling of the sound- — arises when maximal 
arterial filling and collapse no longer occur. Furthermore, the 

1 Auscultatory Blood-pressure Determinations, Arch. Int. Med., August, 1910. 

2 This phase, not mentioned by Korotko-o-, was first described by Ettinger. Wien. 
klin. Woch., 1907, p. 992. 



THE AUSCULTATORY METHOD 



67 



blood-stream becomes slower and the cuff loses its resonating 
quality owing to a fall of tension. According to Macwilliam and 
Melvin, 1 the fourth phase owes its characteristics to the fact that 
external pressure has become insufficient to cause a flattening of 
the circular arterial tube. They believe that maximum arterial 
oscillation occurs, not as stated by Marey and generally accepted, 
at the point at which external pressure in the cuff and internal 
pressure in the artery are exactly counterbalanced, but at the 




Fig. 14. — The auscultatory method. 

point at which external pressure is sufficient to distort the arterial 
tube so as to produce a half-flattening of the artery. The onset 
of this phase indicates the diastolic pressure. 2 

The fifth phase — disappearance of all sound — occurs when normal 
arterial relations are again established. The onset of this phase 
is accepted by some authorities as indicating the diastolic pressure, 



1 The Estimation of the Diastolic Blood-pressure in Man, Heart, 1914, v, 153. 

2 Macwilliam, J. A., and Melvin, G. S., The Estimation of the Diastolic Pressure, 
Heart, 1914, v, 153. 



68 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

although it seems well established that the beginning of the fourth 
phase should be chosen as the criterion. 1 

It occasionally happens that the change from the third to the 
fourth phase is not clearly defined and it is sometimes necessary to 
make several observations before the exact point of change can be 
established. This is, however, not often the case among those who 
are accustomed to the auscultatory procedure. The identification 
of the onset of the fifth phase is much less readily established, and 
even when accomplished is subject to a much greater element of 
personal error. Some recent observations indicate that when we 
are confronted with sudden changes in pressure due to psychic 
influences (observations on students), the fourth phase is more 
consistently established, whereas among hospital patients the 
fifth phase shows less variability. 2 

The actual average duration of the different phases as measured 
in millimeters of mercury was found by Goodman and Howell 3 
to be 14, 20, 5, 6 mm. in the order given. These last-named authors 
have opened up a very suggestive line of investigation in this 
field by measuring the actual duration of the different phases and 
their relation to each other under various pathological conditions. 
In cases of aortic regurgitation and hypertension, for instance, 
the fifth phase is persistent. (In aortic insufficiency a pistol-shot 
sound is often heard over the arteries when no pressure is being 
exerted.) A long third phase indicates a powerful systole. This 
phase is also lengthened in arteriosclerosis even in the presence 
of cardiac weakness. Atypical auscultatory findings are often 
associated with cardiac insufficiency (Krylow). In some apparently 
normal cases all the phases cannot be made out, but in the vast 
majority, although some may be brief, the five phases are distinctly 
remarked. Variations in the strength of successive systoles are 
often better appreciated by auscultation of the partially compressed 
artery than of the precordium "tonal arhythmia." 

1 Lang and Manswetowa, in comparison with the Hurthle spring manometer, 
obtained closely corresponding readings by taking the auscultatory readings at the 
beginning of the fourth phase, Deut. Arch. f. klin. Med., 1908, xciv, 441; Fischer 
also believes that the beginning of the fourth phase represents the diastolic pressure, 
Deut. med. Woch., 1908, p. 1141; Taussig, A. E., and Cook, J. E., Determination 
of the Diastolic Pressure in Aortic Regurgitation, Arch. Int. Med., 1913, xi, 542: 
Warfield, L. M., Studies in Auscultatory Blood-pressure Phenomena, Jour. Amer. 
Med. Assn., 1913, lxi, 1254. 

2 Kilgore, Berkley, Rowe, and Stabler, A Quantitative Determination of the 
Personal Factor in Blood-pressure Measurements by the Auscultatory Method, 
Arch. Int. Med., 1915, xvi, 927. 

3 Trans. College of Physicians, Philadelphia, 1911; Amer. Jour. Med. Sei., Sep- 
tember, 1911. 



THE AUSCULTATORY METHOD 09 

In estimating blood-pressure by the auscultatory method any 
type of manometer — mercurial, aneroid, compressed air — may be 
employed. 

As a general rule a long and intense murmur phase, beginning 
at a high pressure, points to a vigorous heart action. If it increases 
under exercise, we assume that the heart is using its reserve force. 
When the murmur phase disappears under light work cardiac 

in 

Arterial sound 



11213 

mm. Tig. l" 



Fig. 15. — Fast drum. Sudden decrease in size of pulse wave at 4, marking the 
change from clear, sharp tone to dull tone. 




I 

Fig. 16. — Diagrammatic representation of the auscultatory phases (after Galla- 
vardin). 7, arterial tone (muffled); 77, tone and murmur; 777, arterial tone (loud 
and without a murmur); 71', muffled sound. 




Fig. 17. — Showing the relationship between the oscillatory and the auscultatory 
phenomena (Gallavardin). Here the end of the third phase is drawn as corresponding 
to the last large oscillation. 

weakness is implied, while the splitting of the tones of the first 
phase points to a dilated hypertrophy of the ventricle. If the 
sound or the murmur is subject to variations in duration and in 
intensity, cardiac insufficiency is predicated. The non-appearance 
of the murmur phase has a similar significance. 1 

' Tornai, J., Ueber d. diagnostisches Wert d. auskultatorischen Blutdruckmes- 
sungen, in besondere vom Standpunkt der Funktions-pruefung d. Herzens, Zeitsehr. 
f. Phys. u. diSt. Therap.. 1009, xiii, 504 et seq. 






70 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 




Fig. 18. — The new Nicholson sphygmomanometer. Showing the method of con- 
necting the unions A' and B' with the stopcock A and the connection B. The 
needle valve C must be closed, and the stopcock A open as shown in the cut. 
To close the instrument remove the glass tube H, sliding it into the metal holder 
E. Fold the scale down and then remove the metal unions A' and B'. The lid 
can then be made to close by firm pressure on its upper end. The lid cannot be 
closed until the stopcock M has been turned at right angles to the tube, and when 
so turned no mercury can escape. When closed the instrument fits into a morocco 
case containing also the bulb and cuff, and can be carried in the pocket. 

Accuracy is assured: (1) by a millimeter scale, especially compensated for the 
lowering of the level in the mercury reservoir: (2) by the zero (0) point on the scale 
being adjustable to the mercury level, so that the readings are not affected by climate 
and temperature changes; (3) by the scale reading directly in millimeters of mer- 
cury, the primary standard, it does not have to be checked up; (4) by the use of a 
large column of mercury; there is no separation of the mercury, and oxidation and 
capillary errors are avoided; (5) by the use of a steel stopcock and flint-glass no 
amalgam is formed with the mercury, so no friction; (6) by a steel needle valve 
there is a perfect air release. The mercury remains clean owing to a new method 
of preventing powder from the rubber tubes being sucked into the mercury reservoir. 

Portability. (1) All parts are thoroughly protected by a metal case; (2) by a 
special stopcock no mercury can be lost; (3) by stopcock .4 one has an addi- 
tional safeguard should the rubber washer in the pump leak slightly, until it can 
be replaced by a new washer. The mercurial column can be absolutely maintained 
by closing the stopcock. This permits of using the arm band to produce Bier's 
hyperemia. By inflating the apparatus to 50 to 60 mm. Hg. and then closing the 
stopcock A one can maintain the pressure for any length of time desired. This 
is impossible of attainment on any apparatus not having this stopcock. This is 
the only pocket sphygmomanometer which has this special feature. In addition to 
the above the apparatus is simple to operate, using a wide, soft cuff, and ha.- an 
automatic catch on the lid which holds the instrument in the upright position when 
in operation. (Manufactured by the Precision Thermometer and Instrument Co., 
Philadelphia.) 



INSTRUMENTS FOR ESTIMATING BLOOD-PRESSURE 71 

INSTRUMENTS FOR ESTIMATING BLOOD-PRESSURE. 
A. RIVA-ROCCI TYPE. 

The new Nicholson sphygmomanometer is a readily portable 
mercurial column instrument enclosed in a metal case. The lid 
when raised automatically locks in the upright position and acts 
as a support for the instrument (Fig. IS). 




Fig. 19. — Vertical cross-section of Nicholson's new pocket sphygmomanometer. 

We believe this instrument to be the best practical sphygmo- 
manometer yet devised. It is small, accurate, readily portable 
and well constructed. Nicholson has also devised an even smaller, 
more compact, cheaper, and yet accurate instrument — the Princo 
sphygmomanometer — which deserves an equal endorsement. 

This instrument may also be obtained furnished with a Fedde 
indicator (oscillating index), which consists of a vertical tube con- 



72 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 



taining a pith ball, the excursions of which during alternations of 
pressure are both free and extensive, thus affording signal aid in 
determining the diastolic pressure by the visual method (Fig. 52). 

Another instrument of the Riva-Rocci type, long familiar to 
American physicians, is that of Janeway (Fig. 22). It is now 
supplied with a metal needle-valve pump instead of the rubber 
bulb depicted in the cut. 1 





Fig. 20. — Nicholson's Princo sphygmomanometer. The instrument in a semi- 
folded and open position. A, terminal of tubing; B, socket for the same; C, stop- 
cock: D, needle valve; E, clamp level to set scale at proper mercurial level; F, 
mercurial reservoir; G, hinge which permits folding of calibrated standard; H, auto- 
matic valve which permits folding of manometer tube and retains mercury when in 
transit; /, scale folded; K, tubingfolded; N, screw cap to permit removal of mercury. 

The Mercer sphygmomanometer is a mercury instrument the 
form and construction of which are shown in Fig. 23. The instru- 
ment may be clamped to a table or held in the hand while read- 
ings are made. The cuff and bulb are carried separately. 2 

Leonard Hill 3 has devised a compact and convenient form of 

1 Manufactured by Dressier-Beard Mfg. Co., 286 Second Avenue, New York. 

2 Manufactured by A. Kuhlman & Co., 203 Jefferson Avenue, Detroit, Mich. 

3 A New Form of Mercury Sphygmometer, British Med. Jour., February 19, 1910 



INSTRUMENTS FOR ESTIMATING BLOOD-PRESSURE 73 

mercury sphygmometer. It consists of a single graduated tube 
the base of which is sealed into a small reservoir in the lower end 




Fig. 21. — Faught's mercury sphygmomanometer showing relation of parts, metal 
pump, and special expansion tubing for inflator. 




Fig. 22. — Janeway's sphygmomanometer. 



of which it opens (E). The tube leading from the cuff is attached 
to the other end of the reservoir, which contains the mercury. The 



74 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

chief advantages claimed for the instrument arc: (1) The manom- 
eter being of the single tube variety halves the error of reading 



300 




Fig. 23. — The construction of the manometer of the Mercer instrument. A U-tube 
manometer with the top of each limb of the D closed with a barometer kid gasket 
held securely in a metal socket. The gasket allows the air to pass freely but retains 
the mercury. The manometer is enclosed in an outer metal casing tube which is 
slotted and provided with a direct reading scale. The shorter limb of the U is con- 
nected with a slip socket in the bottom of the outer tube by a small metal tube as 
shown. Only glass and kid come in contact with the mercury. 



as compared with the U-tube type. (2) Owing to the capillary 
opening the mercury cannot spill. It can be carried in any position, 



INSTRUMENTS FOR ESTIMATING BLOOD-PRESSURE 75 

requires no rubber caps or stopcocks. (3) Ready portability; no 
box is required; the wooden case, cuff and pump can be carried in 
a handbag (Fig. 24). 

Several inexpensive instruments of the Riva-Rocci type are on 
the market which, especially if the auscultatory method be em- 
ployed, will be found entirely satisfactory for clinical work. Among 




Fig. 24. — Hill's sphygmometer: A, sphygmometer; B, case; C, section of mercurial 
reservoir; D, brachial cuff; E, pump. 



these the instruments of Linnell, 1 Kercher, 2 Cook, 3 Sahli, 4 Bruhns- 
Fahraeus 5 may bementioned. (See p. 133.) 

1 A Pocket Mercury Manometer, Jour. Amer. Med. Assn., October 12, 1912, lix. 

2 Blood-pressure apparatus manufactured by Lander, Cleary & Co., Philadelphia 
:l Cook sphygmomanometer manufactured by the Kny-Scheerer Co., New York. 
4 Manufactured by Biichi & Sohn, Bern, Switzerland. 

6 Manufactured by Stein & Werner, Stockholm. 



76 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

The Gartner tonometer 1 consists of small distensible rubber 
rings which are applied to the finger, and connected with a manom- 




Fig. 25. — Gartner's tonometer. 



eter. The finger is rendered bloodless and the point at which 
the blanched skin becomes rosy is taken as the criterion of the 



» Wien. med. Woch., 1S99, xlix, 1412. 



INSTRUMENTS FOR ESTIMATING BLOOD-PRESSURE 77 

systolic pressure. This instrument yields variable amounts of 
error but is still occasionally employed in connection with brachial 
readings to determine the pressure ratio between large and small 
arteries, in the hope of thus throwing some light on the state of 
vascular tonus (Fig. 25). 




Fig. 26. — Bishop's blood-pressure apparatus. 



" The method of Gartner is open to the objection that the arteries 
of the fingers are probably small enough to participate directly in 
vasomotor changes. Therefore a rise of the general blood- pressure, 
which in part is caused by constriction of the digital arteries, may 
be associated with a fall of pressure in the terminal phalanges. 
That this does occur is practically demonstrated by the fact that 
cold, which usually causes peripheral constriction with consequent 



78 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 



Mg.4. 




Fig. 27 



COMPRESSED-AIR MANOMETERS 79 

rise of the general blood-pressure, seems to cause a fall of pressure 
as estimated by the method of Gartner." 1 

What may be described as a home-made blood-pressure apparatus 
has been devised by Bishop. The accompanying diagram is suffi- 
ciently explanatory to indicate the general principle upon which 
the instrument is based 2 (Fig. 26). 



A. COMPRESSED-AIR MANOMETERS. 

Compressed-air instruments are small, light and compact. A 
small quantity of mercury or colored liquid is kept in the bulbous 
end of the glass tube. When pressure is raised, a drop of this 
fluid is forced up into the glass tube. This is simply used as an 
index by means of which the height of the pressure can be read off. 

The Oliver Instrument. 3 — Method. — Lay the instrument on a flat 
surface and lift the upper end of the manometer by the brass ring, 

1 Erlanger, The Circulation, Jour. Amer. Med. Assn., October 27, 1906. 

2 For detailed description see L. F. Bishop, The Measurement of Human Blood- 
pressure, Arch. Diag., April, 1908. 

3 Manufactured by Dressier-Beard Mfg. Co., 386 Second Avenue, New York. 



Legend for Fig. 27. 

Universal sphygmomanometroscope. At Janowsky's Clinic in Petrograd the 
blood-pressure in the upper extremities is determined by comparison of the findings 
of five different apparatus. These include the Riva-Rocci cuff, the tonometer, the 
two spring manometers of Basch and the water manometer of Zipliaef-Janowsky. 
N. van Westenrijk, of Petrograd, has succeeded in combining these various apparatus 
in a single one in which one mercury manometer answers for all. It is arranged so 
that the zero point can be adjusted, and it allows comparison of the findings with 
different technique and registration of the pressure up to 350 mm. Hg. The mercury 
tube R (Figs. 1 and 3) opens below into the reservoir R', the graduated scale (Figs. 1 
and 4) being fastened within the mercury tube and the reservoir. The whole is 
mounted on a weighted wooden standard. The right-hand branching arm of the 
reservoir R' (Fig. 2) is connected with the tube which forks to the Riva-Rocci cuff 
E (Fig. 1), the Gartner tonometer ring D, the Basch contrivance for determining the 
pressure in the capillaries F, the rubber bulb for determining the blood-pressure in 
the veins G, and the rubber bulb H for increasing the pressure in the glass chamber 
F. All these are controlled with stopcocks in the tubes. The left-hand branching 
tube from the reservoir R' is connected with the rubber bulb A, which is compressed 
by a screw lever to increase the pressure (Fig. 1) in the cuff and ring and also in the 
manometer. The tube B, with its two enlargements and capillary lumen (oscillom- 
eter) runs in the groove K, and is brought into connection separately with the 
cuff, ring, etc., on the other side of the reservoir R', by turning the stopcock C- 
The apparatus allows the Riva-Rocci cuff to be used for tonometry as well as in the 
usual manner. The illustrated description is published in the Mitteilungen der 
Gesellschaft fiir innere Med., 1908, vii, 202. Universal sphygmomanometroscope, 
manufactured by Eberhard, Petrograd, Russia. 



80 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

at the same time opening out the hinged prop at the back to the 
extreme right-hand corner of the box. This places the scale at an 




Fig. 28. — The Oliver mercurial compressed-air manometer. 









,<0 


, ^3 


\ £. ■> 




c^^^ 


JMtt 


\ 


^^ 





Fig. 29. — Hertz sphygmomanometer. 1 

1 Das Neue Modell meines Blutdruckmessers, Wien. klin. Woch., 1911, No. 37, p. 
1306. Kolomoitzew (Munch, med. Woch., July 20, 1909, p. 14S2), although obtaining 
figures within normal ranges with this instrument, found an accurate accordance 
with Riva-Rocci reading in only 13 per cent, of the cases. 



COMPRESSED-A J It MA NOME TERS 



81 



angle of about 45 degrees and facilitates observation. Tempera- 
ture variations are compensated for by the vacuum which sur- 
rounds the pressure chamber. The scale is in millimeters of mer- 
cury, having been standardized. Any mercury remaining in the 
tube may be shaken down, as in a thermometer, when the box is 
closed. A modification of this instrument is made by Tech, of New 
York. The instrument is simple and compact. It consists of the 
usual cuff and inflation bulb. The manometer is of the compressed- 




Fiu. 30. — The Bendick Instrument. Diagram showing the glass tube of the water 
sphygmomanometer: A, bulb partially filled with water on which pressure is exerted 
by a column of air in the tube leading from the cuff; B, level of water in upright 
calibrated tube C, which contains air above; D, bulb in the tube C, to contain the 
air as the water rises. At the top of the tube is a cock for closing the tube after the 
water is put in below. 



air type, a drop of mercury being used as an index. It is open to 
the criticism, however, that the small scale with widely spaced 
gradations militates against accuracy. 

Hertz's Sphygmomanometer. — Method. — After application to the 
wrist as shown in the cut, the cautery bulb / is tensely inflated, 
the clip d cutting off communication with the cuff. When this 
is accomplished the clip d is opened and the droplet of mercury 
approaches the distal end of the manometer. The systolic press- 
6 



82 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

ure is read at the point at which the radial pulse disappears; the 
diastolic pressure, at that at which the pulse becomes diminished 
in volume. 

Bendick's air-water sphygmomanometer 1 is calibrated in millimeters 
of mercury. Water is poured into the reservoir until the points 
A and B are reached. The stopcock is then closed above D. 
The pressure in the cuff is exerted on the fluid at A and transmitted 
to B while the air in the column is being compressed. The bulb 






Fig. 31. — Bendick's air-water sphygmomanometer. 

acts as a reservoir for the fluid, the bulb B for the air, allowing 
the liquid to rise the entire length of the tube in recording pressures 
up to 300 mm. Hg. The two bulbs allow for a larger and more 
accurate scale than is the case where straight tubes are used. 
The metal T-tube with a stopcock and needle-valve escapement 
allows the air pump to be disconnected and controls the fall of 
pressure. 

1 A New Air-water Sphygmomanometer, Jour. Amer. Med. Assn., 1911, lxi, 
1873. Manufactured by Eimer & Amend, 205 Third Avenue, New York City. 



CHAPTER III. 

THE INSTRUMENTAL ESTIMATION OF BLOOD- 
PRESSURE (Continued). 

III. The Graphic Method of Estimating Blood-pressure. — If 

instead of employing the finger below the cuff in order to determine 
the presence and character of the pulse wave, a sphygmograph is 
substituted, one obtains a graphic tracing of the appearance, 
increase, maximum oscillation, and final disappearance of the 
pulse, which occurs while the pressure in the cuff is falling from 
above the systolic to below the diastolic pressure. Such a pro- 
cedure has the advantage of furnishing a permanent record, and 
also of allowing one to judge more accurately the exact point 
at which the maximum pulsation is established. The graphic 
method is therefore employed where the greatest accuracy is 
demanded, as in experimental work. 

In the instruments of Erlanger, Uskoff, Muenzer, instead of a 
sphygmograph on the radial artery, the brachial pulsation of the 
cuff itself is transmitted indirectly to a kymograph. "Indirectly," 
because the pressure in the cuff, were it riot "stopped down," would 
be too great for the delicate membranes connected with the tambour. 

The systolic pressure is determined by noting with a decreasing 
pressure the point at which the first full pulse wave is transmitted 
to the drum. While the cuff pressure is still above this level a series 
of small elevations often appear which are due to the impaction 
of the pulse wave against the upper margin of the cuff, the central 
portion of which still occludes the blood-flow. 

The lower end of the maximum excursions is generally taken as 
an indication of the diastolic pressure because at this point there 
is just sufficient pressure in the cuff to cause a complete diastolic 
collapse of the artery, while at the same time permitting a com- 
plete distention during systole. Pressure on either side of the cuff 
being about equal, although alternate, the greatest oscillation of 
the interposed membrane occurs. Below this level the excursions 
grow progressively less because with the falling manometrical 
pressure less and less of the arterial pulsation is transmitted to 



84 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

the gradually loosening cuff. In some cases it is difficult to deter- 
mine the exact point at which the inframaximal pulsations begin. 

When the diastolic pressure is being estimated by the graphic 
method it sometimes happens that two regions of maximum oscilla- 
tion occur. "The first diminution in amplitude occurs apparently 
at the moment the blood begins to reenter the arm with considerable 
velocity. The amplitude again increases when the vessels of the 
arm become distended with blood." The second maximum is 
undoubtedly the minimum pressure (Erlanger and Hooker). 




Fig. 32. — Pulse tracing made with the Gibson instrument. Here the first full pulse 
wave iS indicates the systolic pressure. It is the first wave which has overcome the 
pressure in the brachial cuff and reached the radial artery. Preceding the point .S 
a number of small waves are seen which are produced by the impact of the pulse 
waves against the upper portion of the brachial cuff, a segment of the artery being 
still obliterated. Tracing taken by rapid inflation and gradual escape with quickly 
revolving cylinder. It shows systolic pressure to be 170; diastolic pressure, according 
to Gibson, 106 (D) ; and by Masing's method, 90 (D'). (Tracing after Gibson.) 



Occasionally a successive series of maximum waves at about the 
diastolic level are observed. This is attributed by Sahli to two 
factors: (1) With increasing compression, when the minimal 
pressure is exceeded, the pulse wave undergoes a stasis underneath 
the (broad) cuff which increases the pulsatile excursions of the 
tonograph. (2) At the same time a continuously diminishing 
amount of the sphygmographic wave becomes available for 
transmission. These effects tend to counteract each other and 



GRAPHIC METHOD OF ESTIMATING BLOOD-PRESSURE 85 

the resulting waves will vary according to which of the two effects 
predominates. Another explanation is that the collapse of the 
artery being gradual, at first only that portion of the artery which 
underlies the centre of the cuff is compressed; some time is required 
before the whole segment is similarly affected (von Recklinghausen). 
According to this argument, with a rising pressure one should choose 
the beginning of the large oscillations as the diastolic criterion. 
This source of confusion may be obviated by the simultaneous 
employment of a brachial and a radial cuff, in which event the 
lower cuff will show a distinct oscillatory diminution the moment 
the diastolic level in the upper cuff is exceeded. 

If the pressure "be allowed to fall more slowly than in von 
Recklinghausen's experiments the maximum oscillations will be 
followed immediately by the abrupt diminution in amplitude — - 
the diastolic pressure corresponds with the abrupt diminution in 
amplitude" (Erlanger). 

"There are obviously two processes at work tending to alter 
the amplitude of the peripheral pulse while the artery is being 
compressed: (1) some unknown factor which tends to enlarge the 
pulse amplitude; (2) the pressure from without must constantly 
tend to diminish the amplitude of the peripheral pulse by dimin- 
ishing the caliber of the artery. It is true that the latter factor 
will not be great so long as the external pressure is less than the 
intra-arterial minimum; the great diminution in caliber will occur 
when the diastolic pressure is exceeded. There is no justification 
for Sahli's assumption that the arteries suffer no lateral expansion 
with the advent of the pulse wave and that therefore the caliber 
of the artery is not diminished by external pressure until that 
pressure exceeds the diastolic" (Erlanger). 

Gibson advised selecting the middle point of the greatest ampli- 
tude of oscillation as the diastolic point (Fig. 36). Strassburger 
takes the point at which the previous maximal oscillation begins 
to diminish under increasing pressure. Macwilliam and Melvin, 1 
who have investigated the relation of the diastolic pressure to the 
maximum oscillation, believe that the latter occurs not at the point 
at which internal and external arterial pressure are equalized, but 
when a " half -flattening" of the arterial lumen is brought about. 

The oscillation, they believe to be compounded of "(a) the dif- 
ference in capacity between the half-flattened and the circular 

1 The Estimation of Diastolic Pressure in Man, Heart, 1914, v, 153. 






86 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

tube, (b) the distention caused by the systolic wave and (c) such 
volume change as may result from longitudinal expansion at each 
pulse beat." The point of maximum oscillation varies greatly 
owing not only to a disturbance in the relationship between the 
components just mentioned, but also owing to (1) distensibility 
and flexibility of the arterial wall, (2) the interval between systoles, 
(3) the form of the internal pressure curve, and (4) the degree of 
arterial elongation at each beat. Finding none of the previously 
mentioned criteria always accurate they suggest taking as the index 
of the diastolic pressure "the level of the external pressure just 
after the abrupt diminution has taken place," that is, the point 
at which pressure is just insufficient to cause flattening of the artery. 

If a tracing is taken from the artery below the seat of compres- 
sion a sphygmographic curve results. In such a curve the onset 
of the large waves is accompanied by a change in the form of the 
waves. At the upper systolic level of the large waves the pulse 
previously anacrotic, becomes katacrotic; at the lower level the 
diastolic wave falls away almost vertically instead of obliquely 
(von Recklinghausen). These facts furnish us with a further 
means of recognizing the diastolic pressure provided we are able 
to recognize the katacrotic notch. 

The diastolic pressure by the graphic method, as shown by 
Miiller and Blauel, may be as much as 2S per cent, too high. 
Although the artery at once increases its oscillations when the 
diastolic level is reached, it takes some time for a complete arterial 
collapse to be established. 

The systolic pressure cannot always be absolutely determined 
because of the primary small subsystolic waves due to concussion 
of the upper border of the cuff. The diastolic pressure cannot always 
be absolutely measured because (1) there is still a difference of 
opinion as to which criterion should be used (beginning, middle, 
or end of the large waves or the onset of. the anacrotic notch), and 
(2) because it is not always possible to determine the exact point 
at which these changes occur. But since it is admitted that clinical 
blood-pressure readings are approximate estimations only, and not 
exact mathematical calculations, the results obtained will be 
sufficiently accurate for practical purposes. 

Since the foregoing lines were written, corroboration of the state- 
ments made has been furnished by the investigations of Kilgore, 1 

1 The Large Personal Factor in Blood-pressure Determinations by the Oscillatory 
Method, Arch. Int. Med., 1915, xvi, 893. 



INSTRUMENTS FOR GRAPHIC REGISTRATION 



87 



who showed that identical tracings made with the Erlanger appara- 
tus were very variously interpreted by different individuals, even 
by those who were familiar with the instrument and who were 
using the same criteria of the systolic and the diastolic pressures. 

Erlanger states that these discrepancies can be minimized if 
not actually obviated by (1) using as the systolic criterion the 
change in form, with the paper moving at sufficient speed for this 
purpose; (2) by using the first consistent decrease in amplitude as 
the diastolic index; and (3) in doubtful cases controlling the read- 
ings made by the method of continuous escapement by readings 
made by that of intermittent escapement. 1 (See page 91.) 

C. INSTRUMENTS FOR GRAPHIC REGISTRATION. 

When using the graphic method, some sort of an automatic 
registering device should be attached to the instrument, for other- 




Fig. 33.- — The Jacquet sphygmotonograph. 

wise one is forced to mark by hand the various pressure levels on 
the moving paper while watching the fall of the manometer, a 
procedure which is always irksome and often inaccurate. Various 
devices have been employed to obviate this necessity by sub- 
stituting an automatic indicator which marks the varying height 
of pressure upon the record. Thus in case of the sphygmoto?wgraph 
of Jacquet 2 (Fig. 33) the stylet of a small metallic manometer 
communicating with the brachial cuff registers directly on the 
tracing. The beginning of the curve represents 50 mm. Hg. and 
each elevation of 1 mm. on the tracing is equivalent to a pressure 
increase of 10 mm. Hg. This device can be attached to the regular 
Jacquet cardiosphygmograph and has the endorsement of Gal- 



1 Erlanger, J., An Analysis of Dr. Kilgore's Paper, etc., ibid., p. 917. 

2 Manufactured by C. & E. Streisguth, Strasburg, Germany. A. H. Thomas & 
Co., Philadelphia agents. 



88 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

lavardin. It is open to the criticism which applies to all metallic 
manometers — the necessity of standardization. 1 

Bingel 2 has devised an instrument in which every pressure 
change of 10 mm. is marked on the tracing by the interruptions of 
an electric current. This spacing is rather wide even for clinical 
purposes. 

The sphygmomanometer devised by G. A. Gibson 3 (Fig. 35). con- 
sists of "a mercurial manometer, the lumen of which is exactly 
that of the ordinary physiological kymograph." The air contained 
in the armlet can be increased, and the pressure on the limb there- 
fore elevated, by means of a large syringe, and the pressure may 
be raised quickly or slowly, according to requirements. By means 
of a valve the pressure may also be lowered quickly or slowly. 




Fig. 34. — Cross-section of the registering metallic manometer of Jacquet. 

A float rests upon the mercury, surrounded, as is usual in the 
physiological laboratory, by alcohol, and an upright rod of aluminum 
leads to a horizontal arm which writes on the revolving cylinder. 
In order to have the absolute zero, a fixed arm traces the abscissa 
upon the cylinder, which is driven by a clock-work placed hori- 
zontally, as in the instrument of Erlanger. The pulsations of the 
artery below the point of compression are recorded by means of a 



1 Silbermann, who has studied the changes which occur in the diastolic portion of 
the sphygmogram during an increasing cuff pressure, believes that some deductions 
can thus be drawn concerning the amount of vascular tonus. Neue Untersuchungs- 
ergebnisse bei d. Blutdruckmessung mittels des Tonographen, Deut. Aerzte-Zeitung, 
May 15, 1909. 

2 Ueber Messung des diastolischen Blutdruckes beim Menschen. Munch, med. 
Woch., 1906, xxvi, 1246. Manufactured by Albrecht, Tubingen, Germany. 

3 Quart. Jour. Med., 1907, i, 103. 



INSTRUMENTS FOR GRAPHIC REGISTRATION 



89 



transmission sphygmograph. This consists of a tambour brought 
into contact with the brachial or radial artery, as may be most 
convenient, by a pelotte resting upon the vessel. It is adjusted 
to the arm by means of a spring provided with a screw. This 




Fig. 35. — Gibson's sphygmomanometer. The recording sphygmomanometer 
described in the text: 1, armlet; 2, manometer; 3, scale; 4> valve for regulating 
pressure; 5, clip, acting as a valve to syringe; 6, inflation syringe; 7, support for 
transmission sphygmograph; 8, pelotte; 9, screw for adjusting sphygmograph to 
artery; 10, clip for arranging pressure; 11, recording lever of manometer; 12, 
weighted thread for adjusting lever; 13, tambour recording movements of transmis- 
sion sphygmograph; H, arm marking abscissa; 15, revolving cylinder; 16, clock- 
work. 



tambour is brought into communication by rubber tubing with 
another tambour, the movements of which are recorded on the 
cylinder simultaneously with the movements of the kymograph. 



90 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

The best tracing is obtained when the tambour in contact with 
the artery is larger than that connected with the recording lever 
by means of which the movements are amplified. The whole 
apparatus is shown in Fig. 35. 

"In using the instrument the pressure within the cuff may be 
raised gradually or quickly, the latter being the more usual course. 
If it is slowly raised, the tracing of the kymograph shows at first 
a line of ascent with small oscillations, but as it rises the pulsations 
become more and more marked, and the excursion of the index 
more extensive, until a maximum point of amplitude is attained, 







Fig. 36. — Tracing obtained by slow inflation and slow continuous escape. The 
ascending curve shows the pressure to be 180 systolic and 120 diastolic. The descend- 
ing curve shows it to be 180 systolic and 118 diastolic. 



when they begin to diminish and gradually disappear. Simul- 
taneously the transmission sphygmograph records a gradual 
diminution in the amplitude of the pulsations, which finally cease. 
When all the movements of the kymograph, as well as of the 
sphygmograph, have come to an end, the pressure is allowed to 
fall by the escape of air from the valve, and the events which follow 
are the converse of those just described." Such a tracing is shown 
in Fig. 36. 

The manometer is of the double column (U-shaped) variety 
and in reading the record the height of the abscissa must be doubled, 
e. (/., actual reading 60 mm., corrected reading 120 mm. 



INSTRUMENTS FOR GRAPHIC REGISTRATION 



91 



If the pressure in the cuff is allowed to fall continuously, the 
oscillating mercury acquires a progressively increasing momentum 
which tends to depress the lowest point of movement beyond its 
true level. This point is well illustrated in Fig. 37, a tracing taken 
by the method of intermittent escapement. In order to obviate 
this, Gibson advocates choosing the mean instead of the lowest 
point of the curve when reading the diastolic pressure. 

The advantage of this instrument over that of Erlanger lies in 
the fact that the height of the mercurial column is automatically 
recorded, and that the personal equation is entirely eliminated. 




Fig. 37. — Tracing taken by rapid inflation and gradual intermittent escape, inter- 
rupted approximately after each descent of 5 to 10 mm. Hg. It shows a systolic 
pressure of 118, and a diastolic pressure of 74. The varying effects of inertia are to 
be observed, as described in the text. (After Gibson.) 



Its disadvantage in relation to the former is due to the inertia of 
the mercurial column which renders it less sensitive to delicate 
pressure changes. A closely -similar instrument has been devised 
by C. Singer, 1 which is better adapted to clinical purposes in being 
less bulky and heavy, without sacrificing accuracy. 
The Erlanger 2 sphygmomanometer is an instrument somewhat 

1 A Clinical Apparatus for Obtaining Graphic Records of Blood-pressure, Lancet, 
February 5, 1910, p. 365. Manufactured by Hawksley & Son, London. The instru- 
ment fits into a case 14^ x 5 x 4 inches, the cuff is carried in the cavity of the cylinder. 
The tracings are made with ink pens upon white paper. 

2 Johns Hopkins Hospital Report, 1904, xii, 02. 



92 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 




To An 



lo Inyia-Vo-r 



Fig. 38.— Erlanger's sphygmomanometer. 



INSTRUMENTS FOR GRAPHIC REGISTRATION 93 

similar to that last described. Owing to its size and construction 
it is better suited for the research laboratory than for the hospital. 
It has the advantage of yielding permanent graphic records, but 
necessitates considerable skill in its employment. 

While somewhat complicated in construction it differs from 
other instruments of this type chiefly in its method of recording 
pulsations. A U-shaped manometer connects by means of a four- 
way tube with (1) the arm cuff; (2) a special stopcock; (3) a rubber 
bulb enclosed in an outer glass bulb. The latter is interposed in 
order to reduce the pressure between the cuff and the delicate 
tambour. Records are made on smoked paper on a kymographion 
by means of an aluminum needle (Fig. 38). The pump consists 
of a Politzer bag, and heavy, rigid tubing is employed. 

Some little time is required to make the records and considerable 
familiarity with the instrument is necessary, but graphic records 
eliminate subjective errors. It can be obtained with polygraphic 
attachments and used to make pulse tracings, but is, so far as the 
blood-pressure is concerned, not automatically recording, i. e., 
the height of the mercurial column must be observed and recorded 
by the operator while the tracing is being made. 

The systolic readings obtained with this instrument average 
5 mm. higher than with the Riva-Rocci method with a broad cuff. 
The diastolic readings correspond within a range of from 5 to 
15 mm. 

The Uskoff 1 sphygmotonograyh (Fig. 39) was devised with the 
intention of supplying a portable instrument which could be used 
both for blood-pressure and for pulse tracings. The latter function 
it excellently fulfils, furnishing good simultaneous tracings of the 
brachial artery and any one other desired pulsation, and requiring 
practically no adjustment. 

Blood-pressure tracings taken with this instrument and auto- 
matically registered by an extremely ingenious escapement device 
are for two reasons not satisfactory. (1) Owing to the smallness 
of the opening which connects the interior of the glass bulb with 
the atmospheric air, large pulsations will transmit relatively more 
of their movement to the tambour than is the case with small 
pulsations. As a result of this, neither the sudden change from 
large to small pulsations (diastolic pressure), nor yet the change in 
the type of the individual waves which should appear at this point 

1 Der Sphygmotonograph, Zeit. f. klin. Med., 1908, lxvi, 1 and 2. Manufactured 
by E. Zimmerman, Leipsic. 



94 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

(see p. 86) are demonstrable (Staehelin and Faustus 1 ). (2) The 
rubber, glass-enclosed balloon exerts variable degrees of tension 
for increasing increments of pressure, largely owing to the effect 
of the silk netting by which it is surrounded (Erlanger 2 ). 

The author, who has used this instrument in practice for several 
years on account of its other excellent features, having long since 
become convinced of the inaccuracy of the blood-pressure tracings, 
has employed it with entire satisfaction as a simple manometer 




Fig. 39. — The Uskofi sphygmotouograph. 

in connection with the auscultatory method. The driving mech- 
anism for the tracing is now furnished with two speeds, and a roll 
of smoked paper 25 meters in length, thus eliminating two of its 
early shortcomings. 

The Uskoff sphygmotonograph simultaneously records the 
following : 

a. Blood-pressure in millimeters of mercury. 



1 Das Verhalten des Blutdrucks beim Menschen wahrend der Erholung von 
Muskelarbeit, Zeit. f. klin. Med., lxx, 444. 

2 Criticism of the Uskoff Sphygmotouograph, Arch. Int. Med.. 1912, ix. 22. 



INSTRUMENTS FOR GRAPHIC REGISTRATION 95 

b. Carotid pulse (or jugular pulse or apex beat). 

c. Arterial pulsation from the upper arm (brachial) at varying 
pressures (systolic and diastolic). 

d. Time in one-fifth second. 

In other words, there are four tracings upon the paper, three 
of which are fixed by the limits of the apparatus, i. e., blood-pressure 
in millimeters of mercury, arterial pulsations at various pressures 
and time tracing, while the fourth record may be taken at pleasure 
from either the jugular vein, carotid artery or apex beat. 



Fig. 40. — Tracing of blood-pressure made with the Uskoff apparatus. The upper 
tracing A represents the pressure in millimeters of mercury, and the tracing is made 
while the pressure is reduced from 200 mm. to 50 mm., each vibration representing 
2 mm. of mercury column, with the one vibration, omitted every 50 mm. The second 
tracing B represents -one taken from the carotid artery and recorded by indicator 
2. This indicator may be used to record either the apex heat or the jugular or other 
vein pulsations at will. The third tracing C is the sphygmotonogram Or the tracing 
of the arterial (brachial) pulse under a falling pressure. With 200 mm. of pressure 
this indicator traces a straight line because of the total obliteration of the pulse. 
At 162 mm. of pressure the pulse reappears and at 92 mm. of pressure has reached 
the lowest point of maximum oscillation. If the float on the mercury column con- 
tinues to sink, the internal pressure is shown to be greater and the vibrations become 
smaller and smaller because of the elastic layer between the cuff and the artery, until 
it disappears entirely. This tracing taken under diminishing pressure constitutes, 
therefore, an accurate record of both the diastolic and systolic pressure. 



Method of Operation. — The cuff M is attached in the usual 
manner to the upper arm and pressure applied by means of the 
bulb B until the pulse disappears. The pressure thus applied 
is first transmitted to the mercury manometer Q, lifting the 
perforated float as the mercurial column rises. At the same time 
it is transmitted to the rubber bulb enclosed in the glass bulb G 
which is in air-tight connection with both the cuff and the man- 
ometer. With the handle of the cock H in the vertical position, 
the air in the glass bulb is expelled through the cock A' 2 which 
is automatically opened at the same time as K l . 

When the pulse has, by application of sufficient pressure, dis- 
appeared, the cock H is turned in the direction of the arrow, 



96 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

which movement connects the glass bulb G with the outside air 
through an exceedingly small opening, and the pulsations appear 
because air pressure in the cuff and manometer is thus slowly 
relieved through the valve V and is divided between the rubber 
bulb and the air in the glass bulb G. The pulsations are at the 
same time transmitted from the air in the glass bulb G by means 
of the third tabulature in connection with the indicator to the 
tracing paper. 

The pressure arising from compression of the rubber bulb B 
13 also transmitted to two small outlets confronting each other 
on the top of the manometer, between which openings the per- 
forated float passes as it rises and falls on the mercury column. 
The small holes in the float are arranged 1 mm. apart with out- 
standing marks. The 50 millimeter gradations are indicated by 
the omission of 1 mm. The passage of the air current through the 
small openings and through the corresponding perforations in the 
float operates indicator 3, and thus graphically records the actual 
pressure in millimeters of mercury at any moment throughout the 
operation. 

Another instrument of the graphic type is that of Silbermann 1 
(Fig. 41). It is comprised of a radial and a brachial cuff, a mercury 
manometer, float, revolving drum for smoked paper, and an auto- 
matic registering device. The latter consists of a vertical arm 
from which comb-like projections extend. These projections are 
regularly spaced at intervals corresponding to 5 mm. Hg. in the 
manometer. When the kymographion revolves a series of parallel, 
horizontal lines — like a ruled page — are drawn on the smoked 
paper upon which the sphygmographic tracing is recorded. These 
parallel lines take the place of a scale on the manometer. The 
instrument is also supplied with a time marker, recording fifths 
of a second, and the driving mechanism with two speeds. 

Method. — The brachial cuff B is applied to the arm, inflated 
just enough to bring the pressure level in the manometer on a 
level with the first tooth of the comb, and then clamped off. The 
heavy, double cautery bulb is now inflated to its maximum capacity 
so that when the clamp is released after the kymograph is set in 
motion, a steady and continuous rise in manometrical pressure 
will result. The radial cuff D, consisting of a small rubber capsule 
held in place by a strap, can be brought under different degrees 

1 Der Tonograph, Med. Klinik, August 30, 1908, No. 35, p. 1347. Manufactured 
by Oehmke, 21 Luisenstrasse, Berlin. 



INSTRUMENTS FOR GRAPHIC REGISTRATION 



97 



of tension by means of a screw. When applied, this is so adjusted 
as to produce the maximum radial oscillation. It is used as an 
indicator of the levels at which with a rising pressure (1) the last 
pulse wave traverses the brachial cuff (systolic pressure); (2) the 
first maximum oscillation occurs (diastolic pressure). Readings 
obtained with this instrument are from 4 to 5 mm. Hg. lower than 
with the Riva-Roeci method, discrepancies which result from the 
weight of the float and the friction produced between the float 




Fig. 41. — Silbermann's tonograph: B, brachial cuff; D, radial cuff; R, radial 
pulse recorder; T, time marker; F, float, indicating height of mercury in manom- 
eter; C, comb to mark 5 mm. spacings on kymograph; M, driving mechanism. 



recorder and the smoked paper. As this error is a constant one 
the author suggests setting the abscissa line on a level with the 
second tooth of the comb (Fig. 42). 

Another graphic instrument has been devised by Brngsch. 1 It 
consists of a U-shaped manometer and a revolving drum covered 
with white paper ruled in centimeter squares, which can be set 
at any level. A registering float superimposed on the mercurial 

1 Zur Frage der Sphygmotonographie, nebst Beschreibung eines neuen Sphygmo- 
tonographen, Zeit. f. Exp. Path. u. Therap., May 30, 1912, xi. 

7 



98 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

column transmits its height and pulsations directly to the drum. 
The latter is set at such a level that the. abscissa of the centimeter 




Fig. 42. — Tracing made -with Silbermann's tonograph showing systolic pressure, 
118 mm.; diastolic pressure, 65 mm. 




Fig. 43. — Brugsch's sphygmotonograph. 



ruling and the zero point of the mercury correspond. Thus the 
actual height of the tracing above the base line, multiplied by 2 



INSTRUMENTS FOR GRAPHIC REGISTRATION 



99 



(U-shaped manometer) gives us the correct reading. The brachial 
pulsations are transmitted by means of rubber tubing to a piston 
recorder and inscribed by means of ink pens upon the drum below 
the pressure curve (Fig. 43). 

A more elaborate and complicated instrument, based on the 
Erlanger principle, is the sphygmoturgograph of Muenzer 1 (Fig. 
44). The tubing S connects pump P with cuff M and is 
interrupted by stopcock h to prevent communication with 
the glass-enclosed balloon B, until this is desired. The tubing 
T connects the balloon with the tambour. When air is pumped 




Fig. 44. — Muenzcr's sphygmoturgograph. 

into the system it reaches the manometer St, the cuff M and 
the balloon B. With the cuff applied to the arm and sufficiently 
inflated, the cock h being closed, the pulsations are transmitted 
from the cuff through the balloon to the kymograph upon which 
they are recorded. The kymograph is supplied with two speeds — 
a slow one for blood-pressure tracings, a rapid one for pulse tracings 
— and a time marker. In order to obtain the greatest and most 
accurate oscillations it is necessary to close both the cocks h and 



1 Apparat. z. objektiver Blutdruckmessung, etc., Munch, med. Woch., 1907, 
xxxvii, 1809; also Ueber Blutdruckmessung, Zeit. f. exper. Path. u. Therap., 1907, iv. 



100 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 




Fig. 45. — Turgotonograph. (Strauss-Fleischer.) 




*-^-AAAh 



'juuuvUlMAJ^ 



Fig. 46. — A, pen used for recording oscillations; B, tracing made with the Brugsch 
apparatus. (Brugsch.) 



INSTRUMENTS FOR GRAPHIC REGISTRATION 



101 



)i in order to exclude the pump and the manometer, since in record- 
ing the pulsations only the cuff and the balloon are necessary. 

A somewhat similar instrument has been designed by Fleischer, 1 
who, however, instead of using the glass-enclosed balloon to diminish 
the force of the pulsations between the cuff and the tambour, has 
constructed a device consisting of a metal cylinder m enclosing a 
celluloid cylinder Sch floated on a layer of oil P. The air enters 
from the cuff through the tube r and finding no means of escape 
imparts its pulsations to the counterweighted lever G at the 
point A, whence a wire D again transmits the motion to the 
aluminum recording needle S. (Figs. 47 and 48.) 




Fig. 47. — Strauss-Fleischer device for damping the force of the pulse wave. 

The cuff shown in the accompanying Fig. 48 is used for the 
transmission of the pulse. It consists of a metallic cylinder L, 
the upper closed end of which is perforated by a tube which connects 
with the polygraphic tambour. Its lower end is closed by means 
of a ''lense" consisting of a rubber capsule G filled with glycerin. 
The cuff is held in place by the straps R and its pressure can be 
adjusted by the thumb-screw Sp. With this cuff tracings can be 



1 Ueber turgotonographische Pulsdruckbestimmung, Berlin, klin. Woch., 1907, 
No. 35, 1108. 



102 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

made of most of the superficial arteries, including the digital and 
temporal vessels. 1 

Bussenius's instrument for the graphic registration of the blood- 
pressure ingeniously eliminates the necessity of a driving mech- 
anism for the strip of smoked paper in the following manner: A 
narrow strip of paper supported in an upright slot, falls by gravity 
past the oscillating tambour. The descent of the strip is delayed 
by the displacement of glycerin around a metallic plunger, which 
is so graded that the strip will fall 1 cm. per second. Both systolic 
and diastolic pressures can be estimated with this instrument; in 
fact, two tracings may be made consecutively on the same strip 
and used to control each other (see Fig. 49). It is merely essential 
that the beginning of the tracing corresponds with mm. pressure 
in the manometer. 2 




Fig. 48. — Cuff used with Fleischer instrument. 

]] T ybamo's instrument 3 is essentially a modification of Erlanger's. 
He, however, uses a divided cuff (4 and 9 cm. broad) which yields 
a more accurate systolic reading, since the impactions of the pulse 
wave against the upper part of the cuff are not transmitted to the 
tambour. The height of the pressure is not automatically recorded. 

IV. Visual (Oscillatory) Methods. — Instruments of this type 
are constructed in association with different kinds of oscillating 
devices which indirectly magnify the fluctuations of the mercurial 
column, or otherwise render the pulsations of the cuff more readily 
perceptible. The oscillatory method is more satisfactory for the 
determination of the diastolic pressure than the method of palpation, 
but less so than that of auscultation. 

1 Zur Methodik der Pulschreibung, Berlin, klin. Woch., 1900, xlvi, 2141. 

2 Manufactured by W. Oehmke, Berlin. 

3 Graphische Blutdruckbestimmurigen bei unrcgclmassijier HerzTvirkunjr, Zoitschr. 
f. klin. Med., 1911, lxxiii, 204-220. 



INSTRUMENTS FOR GRAPHIC REGISTRATIOh 103 




Fig. 49. — Bussenius's sphygmotonogniph. 



104 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 



D. OSCILLATORY INSTRUMENTS. 

The instruments based on this method may be divided into: (I) 
Those which register the height of the pressure, and the degree 




Fig. 50. — Bing's sphygmomanometer: a, mensurating cuff; b, occlusive indicating 
cuff; c, sphygmoscope; d, control valve; e, pump; /, manometer; g, manometer 
escapement; h, sphygmoscope escapement. 




Fig. 51. — The sphygmoscope. (Pal.) 



OSCILLATORY INSTRUMENTS 



105 



of excursion by different devices. (II) Those which indicate 
these two factors upon the same dial. The former usually 
render too high systolic readings. The diastolic pressure as indicated 





"-- ERLANGER 
•.BULB 



IMPROVEMENTS FOR 
FACILITATING THE TAKING OF 
MINIMUM DIASTOLIC PRESSURE 



v_,-TO COMPRESSION BULB 



Fig. 52. — FeddS's oscillometer. This instrument has been modi6ed by R. L. 
Hoobler by using two cuffs with a stopcock connection between them, in circuit with 
the pith-ball indicator. This permits the reading of the systolic as well as the diastolic 
pressure, and yields better results in infants (Nicholson). This oscillatory device 
may be used in conjunction with many types of instruments. It is furnished (at an 
extra cost) with the Nicholson and the Faught sphygmomanometers. 



106 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

by type II is practically similar to that obtained by palpation. In 
type I the readings are somewhat higher. 1 

Class I. — The apparatus of Bing 2 (Fig. 50) consists of a man- 
ometer, pump, two cuffs and a colored liquid indicator somewhat 
similar to that devised by Pal 3 " (Fig. 51). Here the lower cuff b, 




4 j^N*5*** 




Fig. 53. — Widmer's oscillometer. 



substituting the finger in the palpatory method, transmits such 
pulsations as pass the upper cuff a to the colored oil droplets in 
the indicator c. The pressure on either side of the oil droplets 



1 Cordier and Rebattu, Arch. d. Mai. du Coeur, 1911, iv, 737. 

2 Ein Apparat. z. Messung des Blutdrueks bei Menschen, Berlin, klin. Woch., 
1907. No. 22; Blutdruckmessungen bei Menschen, Berlin, klin. Woch., 1906. No. 52. 

3 Ein Sphygmoskop. z. Bestimmung des Pulsdruckes, Zentralbl. f. inn. Med., 
February, 1900, No. 15. 



OSCILLATORY INSTRUMENTS 



107 



being equalized, a very slight pulsation in the cuff produces an 
extensive oscillation in the sphygmoscope. 

The values obtained average 10 mm. higher than with the Riva- 
Rocci method, chiefly owing to the fact that in the last-named 
procedure peripheral contraction of the brachial artery may cause 
a local elevation in pressure without affecting the rest of the 
systemic circulation. This factor is said to be obviated in the Bing 
apparatus by the second cuff. 1 

The Sphygmoscope (Pal). — The capillary tube C-C, containing 
a few drops of colored petroleum, communicates with the tube 
A-B, the left arm of which {A- II) is smaller in caliber than the 




Fig. 54. — Vaquez's sphygmo-signal. 

right {II- B). A is a two-way cock enabling communication to 
be established (through 3 and 4) with two manometrical cuffs, 
e. g., one on the arm, another on the finger. B is an escapement 
cock. The tube 2 communicates with a manometer, while 1 is 
connected with the pump (Fig. 51). 

Method. — After the pressure has been raised in the cuff, II is 
turned 45 degrees, thus closing all communications through the 
four-way cock, whereupon oscillations of pressure are manifest in 
the capillary tube C-C. 



1 z. Werth has devised a somewhat similar instrument, equipped with an oscillator 
which transmits the radial pulsations from a rubber glycerin-containing pelotte 
which can, however, only be used for the systolic oscillations. Ucber d. Messung d. 
Systolischen Blutdrucks auf Optischcn Wege, Munch, med. Woch., 1910, lvii, 1286. 
Manufactured by Oehmke, Berlin, Luisenstrasse, 21, N. W. 



108 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

Widmer's Oscillomanometer. — The first full oscillation (systolic 
pressure), and the maximum oscillation (diastolic pressure), are 
indicated upon the graduated scale, while the actual pressure is 
read from the mercury manometer 1 (Fig. 53). 

Another instrument based on the same principle is the " sphygmo- 
signal" of Vaquez. 2 Here again two cuffs are employed, but with 
a metallic manometer and a different form of indicator (Fig. 54). 

E. ANEROID INSTRUMENTS. 

Class II. — The most accurate aneroid instrument at present 
available is unquestionably that of Pachon. 3 It has recently been 
highly commended by Bachmann, 4 who has made extensive studies 
regarding its accuracy. 

"In estimating the systolic pressure it is customary to observe 
the disappearance of the arterial pulsation at the radial (method 
of Riva-Rocci), occasionally at the brachial below the cuff, at 
any rate always at some distance from the point of compression. 
This method of applying Marey's principle is essentially faulty 
and the results obtained are necessarily erroneous. Indeed, it can 
be shown that while the pulse has disappeared at the radial there 
is a pronounced pulsation in that portion of the brachial artery 
under compression. Pachon, who demonstrated this fact by means 
of his instrument (to be described presently) and by the sphygmo- 
signal of Vaquez, gives the following theoretic explanation of his 
experimental finding: 

" The pulse wave has its origin in the contraction of the ventricle 
and represents a certain amount of kinetic energy. This wave 
of pressure spreads from the root of the aorta to the end of the 
arterial system and in so doing loses energy little by little, owing 
to friction against the sides of the vessels. As the resulting dis- 
tention of the arterial walls is normally extremely slight (Poiseuille), 
very little external work is performed by the pulse wave. If, 
however, a segment of an artery is compressed so that a portion 
of its internal pressure is counterbalanced, that segment will yield 

1 Manufactured by W. Oehmke, Berlin. 

2 For further description see Vaquez, Soc. de Biologie, 1908. 

3 Oscillometre sphygmanometrique a grande sensibilite et a sensibilite constante, 
Comptes rendu de Soc. de biolog., lxvi, 776; also Paris Mfedicale, 1911, xxxi, 122. 
Manufactured by C. Verdin, rue Linne 17, Paris. A. H. Thomas & Co., Philadelphia 
agents. 

4 The Measurement of the Arterial Tension in Man, New York Med. Jour., 
February 4, 1911. 



ANEROID INSTRUMENTS 



109 



to a greater extent to the distending force of the pulse wave and 
the vessel wall will begin to move. In other words, external work 
will be done. The compression may be such that the extent of 
the movement of the vessel wall (hence the amount of work done 
by the pulse wave) will exactly balance the amount of energy 
possessed by the wave. At this moment the pulse wave is entirely 
utilized in performing mechanical work; it is therefore absorbed at 
this point and no pulsation can be felt below it. The blood-flow, 
however, has not been interrupted, the intermittent flow has merely 
been changed into a continuous one. This explains why wide cuffs, 
with a larger area for the absorption of the pulse wave, give lower 
figures than narrow ones. It serves to explain also why the arterial 




Fig. 55. — The Pachon sphygmometric oscillometer. 



pressure in man appears so low in comparison to that observed in 
the other mammalia. Benczur reached practically the same con- 
clusions by the combined use of the Recklinghausen and Gartner 
instruments" (Bachmann). 

Marey's principle for the determination of the minimum or 
diastolic pressure has been more correctly applied, in that the 
oscillations of the compressed artery are transmitted directly to 
the instrument and their amplitude noted. As stated by Pachon, 
however, the instrument which is to reproduce these pulsations 
must have both a great and a constant sensibility. The mercury 
manometer has naturally a constant sensibility, but owing to the 
inertia of the mercury this sensibility is but slight, surely not 
sufficient to enable one to compare differences in the amplitude 



110 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

of oscillations at various levels of pressure. Everyone who has used 
the mercury manometer for the determination of the diastolic 
pressure is impressed with its imperfections for this purpose. A 
few investigators have sought to overcome this defect by placing an 
elastic bag in connection with the cuff, through which combination 
the arteiial pulsations are taken up and transmitted by appropriate 
means to a tambour to be magnified and graphically recorded 
(Erlanger, Uskoff). The first objection to this method is that 
the bag cannot be made sensitive on account of the relatively high 
pressure to which it must be subjected. The second objection is 
that such a bag has not a constant sensibility at various pressure 
levels. The amplitude of its oscillations will be smaller the 




Fio. 5G. — Diagram showing the relation of the essential parts of Pachon's sphygmo- 
metric oscillometer. (After Pachon.) B is a rigid metallic box hermetically sealed and 
containing in its interior an aneroid drum a with which is connected the lever n. 
M is an aneroid manometer which indicates the level of the pressure in the entire 
system. The box, manometer, aneroid drum a, and the cuff are normally in free 
communication by means of the tubes d, e. f. The pressure can be raised in the 
system by means of the pump P; it can be lowered by allowing the air to escape by 
unscrewing the valve s. The cuff and the aneroid a can be cut off from the rest of 
the apparatus by compressing the rubber tube d by means of the compressor c 
(called separator by Pachon). (Bachmann.) 



greater its state of tension (distention), the force of the oscilla- 
tions remaining the same. It will therefore lead to error to 
compare the amplitude of oscillations obtained at various pressure 
levels. 

All these objections have been removed in the simple and 
ingenious instrument devised recently by Pachon. The main 
features in the construction of this instrument, which he names a 
sphygmometric oscillometer, can best be understood by reference 
to Fig. 56. 

The position of the aneroid a is in the interior of the box, and 



ANEROID INSTRUMENTS 111 

the free communication of the interior of the same manometer 
with the box and the cuff have solved the problem of devising an 
instrument which would have both a great and a constant sensibility 
at any pressure level. By reason of this arrangement the same 
pressure is exerted at all times on the external as on the internal 
surfaces of the drum a; hence this drum is always in a position of 
rest or zero tension, except when by compressing c the cuff is placed 
in direct communication with the interior of the drum and any 
change of pressure within the cuff may then act upon it. These 
changes of pressure due to the pulsations of the artery are normally 
very slight, so that the drum a could be made of relatively thin 
metal, hence very sensitive. This sensibility will always be the 
same, no matter what the level of the pressure around the arm may 
be, since it always takes up the pressure changes in the cuff by 
starting from a state of no tension. 

"In using the instrument the cuff is placed around the arm in 
the usual manner. Air is pumped into the system until the pressure 
is well above the normal arterial pressure. The amount of the 
pressure is read from manometer M. The observer now confines 
his attention to the manipulation of valve s and compressor c, 
using preferably one hand only in order to insure free opening 
of the tube d when valve s is opened and closed. If on com- 
pressing c the hand n does not oscillate, valve s is opened and the 
pressure allowed to fall one-half to one centimeter; c is again pressed 
upon and the hand n observed. This maneuver is repeated until 
oscillations of the hand n to the extent of, say, one degree of the 
dial are shown. This moment indicates the return of the pulse 
at the point compressed, and therefore the maximum or systolic- 
pressure there. This is read on manometer M. To determine the 
minimum or diastolic pressure, the pressure in the system is lowered 
in the manner explained above and the compressor c manipulated 
between each lowering of pressure; at the same time the hand n 
is observed and at the moment its excursions are greatest the 
level of diastolic pressure has been reached, and can be read on 
manometer M. This is the most satisfactory instrument I have 
seen for the determination of the diastolic pressure; the oscillations 
are large and the moment of greatest amplitude is clear cut, for 
both immediately before and immediately after this moment the 
oscillations are noticeably smaller." 

"The determination of the systolic pressure in such instruments 
is a vexed question. Erlanger obtains small pulsations with his 



112 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

instrument, as shown by the movements of the lever, before the 
true systolic level has been reached. This he attributes to the 
'hydraulic ram action' of the pulsating proximal stump of the 
artery against the edge of the cuff. Pachon now uses a cuff adapted 
to the wrist, where, on account of the small size of the vessels, and 
the fairly thick edge of the cuff, the danger of this source of error 
should be greatly minimized. The writer observed that an oscilla- 




Fig. 57. — Diagram illustrating the construction of the Tycos aneroid. 

tion of the hand n, equivalent to one degree of the scale, indicates 
the return of the pulse at the point compressed, as controlled by 
the palpation of the artery under similar conditions. To determine 
this point a cuff is placed around the upper arm and one around 
the wrist. The two cuffs are connected with the Pachon instrument 
by means of a Y-tube; a stopcock is placed in the course of each 
tube coming from the cuffs. A pressure is put around the wrist 
equal to the diastolic pressure at this point. When a pressure is 



ANEROID INSTRUMENT* 



113 



applied around the brachial equal to the systolic pressvire and the 
stopcocks and compressor suitably manipulated, no pulsation is seen 
at the wrist. The pressure must be lowered considerably around 
the brachial before a pulsation is indicated at the wrist. If now 
the radial cuff is removed and the brachial systolic pressure esti- 
mated by the ordinary method of palpation of the radial artery, 
it will be observed that the pulse is felt when the pressure around 




Fig. 58. — Showing the construction of the Faught aneroid. 



the brachial is at the same level as when the indicator of the Pachon 
instrument showed an oscillation of approximately one degree, 
when it was in relation with the radial cuff. The following table 
will show the result of a few observations" (Bachmann): 



Systolic pressure in 
brachial artery (Pachon). 
Age. In mm. Hg. 

27 130 

26 125 

33 130 



Pressure in brachial cuff 
at which pulse appears 

at wrist. 
(Pachon.) (Tactile.) 


Diastolic pressure at 
wrist (Pachon). 


105 


105 


80 


105 


105 


90 


110 


110 


90 



114 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

The systolic readings with the "oscillometer" are from 20 to 
40 mm. Hg. higher than with the Stanton apparatus (Riva-Rocci 
method). In the diastolic readings there is less discrepancy. This 
instrument is well suited to ward or office work. It is free from 
error due to personal equation, yields — especially for the diastolic 
pressure — satisfactory results, and is quickly manipulated; but 
its weight militates against its ready transportation, and it is open 
to the objection which applies to all aneroids, namely, the necessity 
of occasional standardization. 

A number of compact little blood-pressure instruments fitted 
with aneroids are on the market. These instruments consist of a 




Fig. 59. — An aneroid instrument in use. (Auscultatory method.) 1 

chamber of corrugated metal which expands under pressure and 
imparts its movement to a calibrated dial. They can be carried 
in the pocket and are free from all danger of spilling the mercury, 
etc. Breakage is also' less likely. They give readings sufficiently 
accurate for clinical work, but they ham to be standardized from 
time to time, as they are apt to get out of adjustment. Unless the 
readings obtained are occasionally checked up with an accurate 
manometer, one can never be sure that the results are not erroneous. 



■Manufactured by G. P. Pilling & Son Co., Philadelphia. A somewhat similar 
instrument — the Rogers "Tycos" sphygmomanometer — is manufactured by the 
Taylor Instrument Co., Rochester, New York. 



ANEROID INSTRUMENTS 115 

What has already been said regarding the size and character of 
the cuff of course applies equally to this type of apparatus. 

Standardization of the Aneroid. — The accuracy of the aneroid 
can be readily tested with an ordinary mercury manometer, if a 
three-way stopcock is used to connect the two manometers with 
a pump. The pressure is raised 5 mm. at a time and the readings 
indicated by the two instruments are compared, thus showing the 
amount of correction which must be applied to the aneroid at a 
given level. 

The von Recklinghausen tonometer, 1 an instrument which has 
found considerable favor in Germany, is based on the principle 
"first introduced into physical science by Bourdon and later 
incorporated into the kymograph of Fick, that if a very shallow, 
curved, elongated air chamber is fixed at one end of the arc with a 
pressure apparatus, while the other is closed, any increase of pressure 
will be made manifest by a flattening or elongation of the arc, 
thereby imparting a certain movement to the end that is free. 
By a very simple device this movement of the air chamber is 
communicated to an axis on which, guarded by a hair-spring, there 
is fastened a long needle whose tip is made to move along a gradu- 
ated scale previously standardized, the final figures being read 
off from the dial." The pressure which is supplied by a long-stroke 
bicycle pump is transmitted from a standard cuff to the dial, the 
graduations of which are equivalent to centimeters of water (Figs. 
60 and 61). 

It is for several reasons desirable that water should be adopted 
as a standard for measurement rather than mercury, and possibly 
this will sooner or later come to pass. First of all, pressure values 
can be directly translated into grams; second, water and blood 
have nearly the same specific gravity; so that calculations can 
readily be made as to differences in pressure at different levels 
of the body by simply measuring the difference in height in centi- 
meters, e. g., blood-pressure at cardiac level 140, at level of spleen 
140 - 20 = 120. 

Water having less inertia than mercury, and being used as a 
unit in many other connections, would undoubtedly be more desirable 
as a standard for blood-pressure. Unfortunately, however, nearly 
all blood-pressure readings have been made with mercury, so that 

1 Unblutige Blutdruck Messung, Deut. Arch. f. exp. Path. u. Phar., 1906, lv. 
Manufactured by C. & E. Streisguth, Strasburg. A. H. Thomas & Co., Philadelphia 
agents. 



116 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

not only is nearly all the literature based on this standard, but we 
have come to think of blood-pressure in millimeters of mercury. 
A transposition of values from mm. Hg. to cm. H 2 is not readily 




Fig. 60. — The von Recklinghausen tonometer; A, cuff; B, pump; C, tonometer 

dial. 




Fig. 61. — Tonometer. 



ANEROID INSTRUMENTS 



117 



made without reference to a special table. This is one reason why 
the instrument has never found favor, in this country at least. 
It is perhaps a pity, but we are confronted by a fact. Another 
reason lies in the construction of the instrument. It measures 
tension by means of a metallic spring which perhaps even more 
often than in the case of aneroids requires "control" and occasional 
correction to insure accurate readings. 

The systolic pressure as recorded with this instrument is slightly 
above the actual pressure. The diastolic pressure, especially if 
the pulse pressure be large, is too low. Strassburger 1 suggests that 
observations be based both on oscillation and on palpation; and 




Fig. 62. — The new von Recklinghausen tonometer. 



further, that not only the extent of the excursion be used as a cri- 
terion of the minimum pressure, but also the point at which the 
needle begins to "hesitate" and to "tremble." He believes that 
in this manner the error due to the arterial elasticity (which varies 
in individuals, and for different degrees of pressure), as well as that 
resulting from partial loss of pulsation, due to imperfect transmis- 
sion from the cuff, may be mutually controlled. 

The Recklinghausen instrument has recently been modified, 
making it smaller in bulk (21 by 9 cm., weighing f kg.) and more 
readily transportable. It is also supplied in another modification 



1 Weitere Untersuchungen u. d. Messung d. Diastolischen Blutdruckes beini 
Menschen, Dent. med. Woch., 1909, xxxiv, 56 and 100. 



118 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

for office use, with a good-sized compressed-air tank, so that very 
rapid inflation of the cuff is made possible by the release of a screw- 
valve, and repeated estimations may be made without renewing 
the air supply in the tank. Care must of course be exercised when 
releasing so high a pressure lest the limits of the instrument be 
overstepped and the metallic spring be thus permanentlv damaged 1 
(Fig. 61). 

Tables of Relative Values. 
To convert centimeters water into millimeters Hg. 



Cm. 


Mm. 


Cm. 


Mm. 


Cm. 


Mm. 


Cm. 


Mm. 


Cm. 


Mm. 


w. 


Hg. 


w. 


Hg. 


w. 


Hg. 


w. 


Hg. 


w. 


Hg. 


1 


1 


10 


7 


110 


81 


210 


155 


310 


229 


2 


1 


20 


15 


120 


89 


220 


162 


320 


236 


3 


2 


30 


22 


130 


96 


. 230 


170 


330 


244 


4 


3 


40 


30 


140 


103 


240 


177 


340 


251 


5 


4 


50 


37 


150 


111 


250 


185 


350 


258 


6 


4 


60 


44 


160 


118 


260 


192 


360 


266 


7 


5 


70 


52 


170 


125 


270 


199 


370 


273 


8 


6 


80 


59 


180 


133 


280 


207 


380 


280 


9 


7 


90 


66 


190 


140 


290 


214 


390 


288 



10 7 100 74 200 148 300 221 400 295 

To convert millimeters Hg. into centimeters water. 

Mm. Cm. Mm. Cm. Mm. Cm. Mm. Cm. 

Hg. w. Hg. w. Hg. w Hg. w. 



1 


. 1 


10 


14 


110 


149 


210 


285 


2 


3 


20 


27 


120 


163 


220 


298 


3 


4 


30 


41 


130 


176 


230 


312 


4 


5 


40 


54 


140 


190 


240 


325 


5 


7 


50 


68 


150 


203 


250 


339 


6 


8 


60 


81 


160 


217 


260 


352 


7 


9 


70 


95 


170 


230 


270 


366 


8 


11 


80 


108 


180 


244 


280 


379 


9 


12 


90 


122 


190 


257 


290 


393 



10 14 100 136 200 271 300 407 

The Potain instrument has never found favor in this country. 
It is generally and justly regarded as inaccurate, partly on account 
of its construction and largely on account of its application. It 
is still frequently used in France, however, with the idea of com- 
paring the pressure in different arteries — radial, temporal, dorsalis 
pedis, etc. The pressure required to obliterate the pulse is applied 
directly over the artery, the compression being exerted upon the 
pelotte with the fingers. Thus it is very easy to exert the pressure 
mainly against the tissues and but slightly if at all upon the artery. 

Francois Frank- has designed an instrument (sphygmopalpeur) 
for the transmission of arterial or venous pulsations without circular 

1 v. Recklinghausen, H., Neue Apparat. z. Messung des arteriellen Blutdrucks 
beim Menschen, Munch, med. Woch., 1913, lxi, 869. 

2 Conipt. Rend. Soc. Biol., 1909, lxviii, 525; Soc. Biol., Paris, July 25, 190S, p. 226. 



ANEROID INSTRUMENTS 119 

fixation, and recommends its use in connection with the Potain 
sphygmomanometer. It consists of a Marey tambour which is 
attached to an upright stand through a series of levels and joints 
so that it can be set at any angle or direction, the pressure exerted 
by it varied at will. Contrary to the usual findings, he obtained 
higher readings with the Riva-Rocci instrument, a fact which he 
explains as follows. 

"The Potain apparatus acts only on the radial artery, while the 
method of circular compression by producing venous stasis reduced 
the amplitude of the arterial pulse and has the effect of counter- 
pressure, thus yielding too low a reading." 

The sphygmomanometer of Bouloumie consists of a combina- 
tion of the Potain and the Gartner apparatus. It has been used 
in an effort to study the relationship of arterial and capillary 
pressure. 1 

V. Subjective Method. — The subjective sensations of the patient 
may also be used to determine the systolic and diastolic readings. 
With the cuff and manometer applied in the usual manner the 
patient is told to notice the onset of throbbing in the arm below 
the cuff — this indicating the systolic pressure. The disappearance 
of the pulsatory sensations corresponds to the diastolic pressure. 
Quite accurate readings may thus be sometimes attained, but the 
procedure introduces a considerable and quite unnecessary amount 
of the personal equation, and is therefore rarely employed. 

Francois Frank 2 in contrasting the findings of the subjective 
method with those obtained by the Gartner instrument, found 
that the two phenomena (recoloration and sense of pulsation), 
although identical as regards the height of manometric pressure, 
are not so as regards time when compared to the beginning of the 
elevation of a volumetric curve, there being a temporal difference 
of from 4 to 6 seconds between the two. This emphasizes the 
importance of allowing pressure to fall slowly. He suggests that 
the pulsatile phenomenon, which manifests itself later than the 
beginning of recoloration, indicates when at its maximum the 
minimum pressure in the collateral arteries of the fingers; while 
the recoloration and the initial swelling is the index of the maximum 
pressure of the arterioles. He finds that the maximal digital arterial 

1 Bouloumie's instrument described: Amblard, These de Paris, 1907, No. 261, 
p. 51. 

2 La sphygmomanometrie digitale par le precede de Gaertner avec et sans anemic 
prealable, etc., Compt. Rend. Soc. Biol., February 5, 1910, p. 234. 



120 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

pressure is often approximately two-thirds that of the radial press- 
ure, although this relationship is by no means a constant one. 

Methods of estimating pressure based on subjective sensations 
are entirely too inaccurate to be of much use. This applies no less 
to recent refinements than to the method suggested by von Frey, 
which consisted in submersion of the arm in mercury and the meas- 
urement of its depth to the point at which the greatest pulsation 
was felt. 

Comparative Values. — The •palpatory (Riva-Rocci) method yields 
results which are on the average 7.5 mm. Hg. higher for every 100 
mm. Hg. than the actual intra-arterial pressure, and 5 per cent, 
lower readings than are obtained by the graphic method, because 
a certain amount of arterial distention must occur before the pulse 
can be palpated. If a sphygmograph or a second (radial) cuff is 
used to determine the return of the pulse instead of the finger, 
somewhat higher readings (10 to 15 mm.) will generally be obtained. 
The end of the maximum oscillation (diastolic pressure) can be 
more readily determined by this means than by palpation, especially 
in case of the novice. 

The auscultatory procedure yields results which are closely com- 
parable to the graphic method, provided that the fourth phase 
(muffling) and the last of the large oscillations be chosen as the 
criteria of the diastolic pressure (Lang and Manswetowa, Bickel, 
Warfield, Schrumpf and Zabel, Engle and Allen). If the fifth 
phase is chosen Windle found that the results corresponded within 
5 mm. In the average case it will not make more than this degree 
of difference whether we choose the fourth or the fifth phase, but 
in cases with a long fourth phase the discrepancies may amount 
to 10 to 12 mm. With a little training the fourth phase is quite as 
readily recognized as the fifth. The vast majority of cases show 
readings 5 mm. higher by auscultation than by palpation. 

The oscillatory (visual) method tends to yield higher values (5 
to 10 mm.) than that of palpation, and figures practically identical 
with the graphic method (Schriunpf and Zabel). It has a distinct 
field of utility in taking the pressures of infants and individuals 
with very small pulse pressures. The greatest discrepancies occur 
in arteriosclerotic cases. 

The graphic method is more time-consuming and troublesome 
than the other methods, but in the hands of those who are familiar 
with its technique is the most exact. It is generally accepted as 
a standard of clinical accuracv. The actual readings are con- 



ANEROID INSTRUMENTS 121 

siderably higher than the endo-arterial pressure. The margin of 
error may be as high as 25 per. cent. 

On close analysis Zabel found that when well-marked discrep- 
ancies existed between the findings of different methods, the phase 
of "large oscillations" was long, whereas in the class in which the 
results were closely in accord, this phase was brief. Careful observa- 
tion, he believes, shows that the phase of large oscillations really 
consists of two distinct parts. In the beginning the first large 
oscillations exhibit a crescendo quality which bespeaks the increasing 
pressure in the edges of the cuff. Following this in some cases a 
second increase in the oscillation abruptly occurs, which corresponds 
to the Ehret phenomenon and to the beginning of Korotkow's 



Fig. 03. — The diastolic pressure as determined by different methods. (Bickel.) 

third phase. According to this conception the first of these two 
diastolic phenomena occurs when the central portion of the arterial 
lumen is collapsed; the second, when the entire lumen is obliterated. 
Thus the: 

First critical point = onset of large oscillations = beginning 
of fourth auscultatory phase = collapse of central arterial wall. 

Second critical 'point = onset of maximum oscillations = Ehret's 
phenomenon = third auscultatory phase = complete arterial 
occlusion. 

In corroboration of this hypothesis are the facts that (1) in 
brachial arteriosclerosis Ehret's phenomenon is of gradual, not 
sudden, onset; (2) lacks in its brusque quality, and (3) is some- 
times entirely absent. 



122 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

RELATIVE ADVANTAGES OF THE DIFFERENT METHODS. 

In order to obtain the greatest accuracy (as in experimental 
work) and for the purpose of having permanent demonstrable 
records the graphic method excels. 

For routine clinical work where simplicity and celerity, com- 
bined with reasonable accuracy, are the chief desiderata, the auscul- 
tatory method is to be preferred. The older palpatory method offers 
more chance for error, due to the personal equation, and with it 
much more difficulty is experienced in determining the diastolic 
pressure. Furthermore, the auscultatory method has to a con- 
siderable extent eliminated the question, "Which sphygmoman- 
ometer shall I buy?" Because with the last-named method any 
accurate manometer, if supplied with a suitable cuff, etc., will 
answer the purpose. 

The sphygmographic attachment at the wrist, aside from being 
troublesome to adjust, results in venous stasis, which elevates 
the curve and diminishes the excursions. The oscillatory devices 
have the disadvantage that the eye has to measure two different 
points at once. They are useful, however, when the pulse is small, 
and some of them can be used to register the pulsation in the smaller 
arteries. So far as clinical accuracy is concerned, it is not of great 
moment which method is employed. The results will generally 
not vary more than 10 mm. Hg., figures well within the range of 
allowable error. These clinical methods are after all only relative 
estimations, and if the same instrument is used on all cases, and 
the examiner is conversant with the technique, the results will be 
sufficiently accurate for comparison and for practical purposes 
generally. 

Sources of Error. — There is a more or less prevalent impression 
that marked errors in the clinical determination of blood-pressure 
may be brought about through the varying influence of the soft 
tissues surrounding the artery, such as the size and muscular 
development of the arm. 

In the investigations of Muller and Blauel, 1 conducted on arms 
about to be amputated and controlled by manometrical pressure, 
readings from the artery directly showed that the broad cuff gave 
a reading about 10 mm. higher than the actual pressure, a margin 



1 Zur Kritik des Riva-Roecischen u. Gartnerschen sphygmomanometers, Dent. 
Arch. f. klin. Med., 1907, xei, 517. 



RELATIVE ADVANTAGES OF THE DIFFERENT METHODS 123 

of error which waxed larger as the width of the cuff was decreased. 
Hut both Hensen 1 and Janeway 2 have reported cases with very 
great differences between the soft parts of the two arms (atrophy 
flaccidity against hypertrophy) which yielded identical readings on 
the two sides. Certainly if an error exists it lies well within the 
limits of daily physiological fluctuation, provided a cuff with a 
width of 12 cm. is employed. 

The extent of the role played by hypertonicity of the arterial wall 
in causing erroneous blood-pressure readings has been much dis- 
cussed. It has been claimed that some of the excessively high 
readings occasionally obtained in man (350 mm. or over) could 
not represent the actual endovascular tension, but must be due 
to resistance of the arterial wall. 

The subject has recently been reviewed and studied in a series 
of ingenious experiments by Janeway and Park, 3 who found that 
although the arterial wall does offer definite resistance to com- 
pression, greater in large, thick-walled vessels, yet this resistance 
in a normal adult brachial is equivalent to only a few millimeters 
of mercury. In children it is an entirely negligible factor, and in 
adults with a normal blood-pressure the error thus introduced into 
clinical blood-pressure measurements is not greater than 10 mm. 
Hg., "a figure less than the spontaneous variations in pressure 
from minute to minute." 

"Atheroma, even of considerable degree, is without appreciable 
effect on the compressibility. Calcification of the arterial wall, 
when segments longer than 6 cm. are examined, increases only 
moderately its resistance to compression. The overpressure 
dependent on this factor in our experiments did not exceed 17 mm. 
Hg. In clinical blood-pressure determinations, if a wide arm-piece 
be used, and the return of the first fully developed pulse wave be 
taken as the index, as recommended by von Recklinghausen, even 
advanced arterial thickening and calcification probably do not 
introduce an error of any importance. The only factor altering 
the compressibility of an artery which seems capable of introducing 
an error of real importance in the clinical measurement of systolic 
blood-pressure is the state of contraction of the arterial walls. 

1 Beit. z. Physiol, u. Path. d. Blutdrucks, Deut. Arch. f. klin. Med., 1900, Ixviii, 
443. 

2 Influence of the Soft Tissues of the Arm on Clinical Blood-pressure Determina- 
tions, Arch. Int. Med., 1907. 

3 An Experimental Study of the Resistance to Compression of the Arterial Wall, 
Arch. Int. Med., November, 1910. 



124 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

It is impossible from our experiments on surviving ox arteries to 
set definite numerical limits for this in man. From these experi- 
ments, however, combined with our study of human arteries 
after amputation and postmortem, we feel that a degree of hyper- 
tonic contraction of the brachial artery sufficient to cause an error 
of more than 30 mm. Hg. seems improbable, and of more than 
60 mm. incredible, during life" (Janeway). 

Practically all the evidence at hand supports the foregoing 
statements. The latest corroboration is furnished by Macwilliam 
and Kesson, 1 who found that relaxed arteries (Ringer's solution, 
manipulation, sodium fluoride) with normal or thickened walls 
yielded only trivial degrees of resistance to compression. Thickened 
arteries from old animals, especially when contracted (barium 
chloride, epinephrin) below the body temperature, were capable of 
exerting considerable resistance. In the smaller arteries constric- 
tion was sometimes sufficient to resist a passage of fluid at 440 
mm. Hg. Arterial contraction in such arteries could be greatly 
diminished by repeated or long-continued compression and by 
massage of the artery. This procedure, they suggest, may be used 
to determine how great a percentage of a high pressure is due to 
vascular resistance, although it does not enable one to determine 
whether this vascular resistance is due to arterial contraction or 
to other causes. 

They have further shown that soft spots in the course of an 
irregularly sclerosed artery are not bridged over by the brachial 
cuff but that the latter acts effectively even in very limited soft 
areas, thus preventing the resistance offered by the rest of the 
artery from having any great effect upon the readings of the 
instrument. 

Much stress has been laid by some investigators upon variability 
of the conduction of the pulse ware due to alteration in the arterial 
lumen and changes in the resiliency of the arterial wall. Thus 
Hill believes that systolic pressure readings are affected by (a) 
the actual maximum pressure of cardiac systole; (b) the conduction 
of the pressure wave to the periphery. The resistance of the arterial 
wall to compression affects the systolic index of blood-pressure 
but little, but the relative hardness or softness of the vessel affects 
the conduction of the systolic wave considerably, especially if 



1 The Estimation of Systolic Blood-pressure in Man with Special Reference 
to the Influence of the Arterial Wall, Heart, 1913. iv, 270. 



PRECAUTIONS TO BE OBSERVED IN TAKING READINGS 125 

it is large. The force of the wave is damped down in soft arteries 
as sound waves are damped by velvet. 1 

Most of the experimental evidence, however, indicates that 
constrictions of the artery sufficient to cause any considerable 
diminution of conduction can hardly occur between such large 
vessels as the aorta and brachial artery; and further, that increased 
arterial rigidity is equally insufficient to cause an important source 
of error. The difference in pressure obtained in arm and leg, or two 
arms or two legs, is the result of pressure differences in the arteries 
in question, and not due to abnormal conduction of the aortic 
pressure. 

The elasticity of the aorta and its branches is important in 
causing a lower systolic and a higher diastolic pressure in the 
systemic arteries than would a rigid tube, but in blood-pressure 
estimations by the obliteration method, the resiliency of the inter- 
vening arterial tube appears to be negligible. 2 

PRECAUTIONS TO BE OBSERVED IN TAKING READINGS. 

Blood-pressure readings should, for purposes of comparison, 
always be taken in the same (preferably the horizontal) posture. 
At all events the position should be such that the reading is made 
at a point about on a level with the heart, thus eliminating the 
error due to the weight of the blood-column. When possible, 
observations should be made about the same time of day and in 
the same relation to meals. They should not be taken during 
excitement, after exercise, or shortly after the patient has partaken 
of hot food or drink, tea, coffee or alcohol, and not when the ex- 
tremities are overheated or chilled. All- muscular activity on the 
part of the patient must be prevented and complete relaxation, 
both general and local, obtained. Observations made under condi- 
tions of spasm — subsultus, tetanus, etc. — are absolutely unreliable. 
Edema of the tissues is also a fertile source of error, and readings 
obtained from anasarcous patients are of no value. Fear, excite- 
ment or psychic effort have a marked effect on the blood-pressure. 
In taking one's own pressure, higher results are often found than 
those obtained by another observer immediately before or after- 

1 Hill, L., Measurement of Systolic Blood-pressure in Man, Heart, 1910, i, 73; 
Hill and Rowlands, Heart, 1912, iii. 219. 

2 Macwilliam, Kesson, and Meloin, The Conduction of the Pulse Wave and its 
Relation to the Estimation of Systolic Blood-pressure, Heart, 1913, iv, 393 



126 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

ward, simply as the result of psychic concentration. Schrumpf 
relates an instance in which the anticipation of an austere prognosis 
raised the pressure of a patient 33 per cent., to fall again promptly 
when reassurance was forthcoming, and only to rise once more 
when complaining of his insomnia and worries. Gibson found that 
his own pressure was increased 35-40 mm. after delivering a lecture. 
Due allowance for variability of the systolic pressure must always 
be made in neurotic patients. 

Von Recklinghausen observed in his own case a rise of 14 cm. 
H 2 caused by the entrance into his presence of a person whom he 
intended to berate (see Physiological Variations). Putermann 1 
found that the anticipation of an examination almost without 
exception raised both blood-pressure and pulse rate in school- 
children. In extreme cases, psychic states may cause a rise of 90 
mm. Hg., generally in association with marked pleasure, anger, 
or fright. The diastolic pressure in these cases is practically 
unaffected. 2 The interposition of a thin undergarment between 
the cuff and the arm is unobjectionable, in fact, may be positively 
beneficial. In cold weather a chilly cuff applied to the arm, both 
by the displeasure it causes the patient, and by the stimulating 
effect it has upon the vasomotor nerves, may yield erroneous 
readings. In very high-strung individuals it is best to warm the 
cuff before applying it. 

It sometimes happens that the initial systolic blood-pressure 
reading on a given subject yields distinctly higher figures than can 
be obtained in subsequent attempts. Gallavardin and Haour 3 
found, in the study of 100 cases, that this initial high pressure, 
which may amount to 35 mm. in women and 25 mm. in men, may 
last fifteen minutes, although in 50 per cent, of these cases the 
normal point was reached at the end of five minutes. Only the 
systolic pressure was affected, the diastolic level remaining con- 
stant. These figures are certainly high. 

Such an increased pressure may be due to: (1) Psychic influences 
— excitement or fear, chiefly noted in high-strung individuals. 
(2) Pain — arising from the forcible inflation of the cuff on sensitive 
arms or in cases of marked hypertension. (3) Local stimulation 

1 Ueber d. Beeinflussung d. Zirkulationssystem durch d. Schulexamina, Wien. 
med. Woch., 1904, liv, 265. 

2 Schrumpf, P., Die psychogene Labilitiit des Blutdrucks u. ihre Bedeutung in 
d. Praxis, Deut. med. Woch., 1910, xxxvi, 2385. 

3 Baise systolique de la tension arterielle au moment de la mensuration, Arch, de 
Mai. du Cceur, etc., 1912, v, 81. 



THE PERSONAL EQUATION OF THE EXAMINER 127 

of the vasomotor nerves from pressure. (4) Prolonged application 
of the cuff. This tends to relax the artery, and by reflexly dimin- 
ishing the force of systole, possibly lessens the conduction of the 
pulse wave. It also produces marked increase in the venous pressure 
and congestion of the tissues below the cuff. 

Attention has been called to the fact that in estimating the 
diastolic pressure by increasing the manometer pressure, different 
results are sometimes obtained than when the diastolic index is 
taken during a falling manometric pressure, especially if the press- 
ures are gauged on both arms simultaneously. A comparison of 
the diastolic values with a rising pressure may thus indicate an 
abnormal tendency toward blood-pressure variation in a given 
individual. 1 

THE PERSONAL EQUATION OF THE EXAMINER. 

Schultze 2 found that ordinarily with a trained observer a series 
of ten successive measurements will yield a fair average of accuracy. 
Much closer correspondence in successive readings is obtained if 
the manometer is read and the pulse palpated by the same person, 
than if these duties are relegated to two individuals. This results 
from the strained mental attitude of the palpator who is almost 
certain to become "the dupe of expectant attention," knowing 
that his sense of touch is being "controlled" and fearing lest, after 
all, he fail to feel the first pulse wave. His sense of perception being 
therefore raised to its maximum, it often happens that he becomes 
subjectively conscious in his finger tips of his own pulse, especially 
if, as is necessary for accuracy, the manometric pressure is allowed 
to fall but slowly, and the procedure is therefore prolonged. Sub- 
jective appreciation of the pulse is more marked in the second 
finger, and in certain individuals. It is generally perceived from 
ten to thirty seconds after the finger tips of a dependent hand have 
been lightly placed upon a solid object (e. g., table). This factor 
is in our experience only rarely a cause of confusion. 

The frequency with which the subjective pulse appears in "con- 
trolled" observers indicates how variable is the acuteness of our 
tactile perception. If the pressure is read and the pulse is palpated 

1 Macwilliams, J. A., and Melvin, G. S., The Significance of Blood-pressure 
Readings in Man, Brit. Med. Jour., 1914, p. 777. 

2 Ueber d. psychologischen Fehlerquellen bei d. palpatorischen Bludruckmes- 
sung nach Riva-Rocci u. v. Recklinghausen, Arch. f. d. ges Physiol., Bonn, 1908, 
cxxiv, 392. 



128 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

by the same individual the discrepancies of successive readings 
will be far smaller, owing to the subjective suggestible element 
(expectant attention). The first reading having yielded a definite 
result, we consciously or unconsciously "expect" the pulse to 
reappear at about the same level. This is illustrated by Schultze 
in Fig. 64, which shows how much more closely the results of ten 
consecutive readings corresponded when the suggestible element 
is not eliminated. 



140 



130 



IV 




Fig. 64. — In the first two estimations, J and 27, the manometer was observed while 
feeling the pulse wave. In the last two, III and IV, the manometer was not read 
until after the pulse wave had been perceived. 



In the first two estimations, I and II (10 each), the examiner 
observed the manometer while feeling for the pulse wave; in the 
last two, III and IV, the manometer was not read until after the 
pulse wave was perceived. 1 When the suggestible element was 
eliminated, successive readings tallied less closely. 

Another possible source of error lies in the fact that the threshold 

1 Schultze, ueber d. psychologischen Fehlerquellen dei d. palpatorischen Blu- 
druokmessung nach Riva-Rocci u. v. Recklinghausen, Arch. f. d. ges Physiol., 
Bonn. 1908. cxxiv, 392. 



THE PERSONAL EQUATION OF THE EXAMINER 129 

of perception for the appearing and disappearing pulse are not the 
same. In the former we judge of a subsensible stimulus which 
is being raised to, in the latter of a sensible stimulus which is 
being lowered beyond, the point of perception. The point of 
disappearance is definitely more difficult to determine. Finally, 
the mercury in the manometer rarely if ever rises or falls so gradually 
that the examiner has time to decide for each individual millimeter 
of pressure whether or not a pulsation is present. Therefore our 
measurements are for subjective reasons generally exact only within 
3 or 5 mm. Hg. 

In order to minimize all these sources of error the following pro- 
cedures should be adopted: (1) Discard the result of the first 
reading, using it simply to demonstrate the harmless and painless 
character of the procedure; and when possible make subsequent 
readings after some little time has elapsed. (2) Avoid making 
blood-pressure estimations when the subject is excited, anxious or 
worried, as a result of the examination, etc. (3) Make several 
consecutive readings and if they correspond more or less closely, 
take the arithmetic mean. (3) Make the observations as quickly 
as is consistent with accuracy; do not look at the manometer until 
the pulse is felt — at this point the air escapement should be tightly 
closed until the reading is made. (4) Allow the pressure to fall to 
zero between observations, and permit sufficient time to elapse 
between readings for the venous pressure (stasis) to fall to the 
normal level. Never make a reading with a broken mercurial 
column, and be sure that the mercury corresponds with the zero 
on the scale before inflation. Needless to say, most of these sources 
of error are eliminated by using the auscultatory method which 
has therefore come into merited favor. 

In certain forms of eardiac arhythmia, especially auricular fibrilla- 
tion and extrasystole, it becomes very difficult to gauge the blood- 
pressure, as the pulse is never equal in volume or in tension for 
many consecutive beats. A rough estimate of the actual pressure 
may be obtained by measuring first the strongest and then the 
weakest pulsations and thus establishing an average. (See Auricular 
Fibrillation.) 

Possible Accidents. — In certain dyscrasic states — purpura, hemo- 
philia, etc. — too prolonged application of a highly inflated cuff 
may cause capillary hemorrhage. This is very rarely the case. 

Mohr has reported thrombosis following repeated blood-pressure 
observations in a patient suffering from tuberculous pneumonia. 
9 



130 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

This is, we believe, the only case of the kind on record. Hill has 
reported edema in a paralytic arm following the application of the 
cuff in a case with a blood-pressure of 220 mm. 

THE VALUE, ACCURACY AND SIGNIFICANCE OF BLOOD- 
PRESSURE ESTIMATIONS. 

Blood-pressure readings furnish us with important and valuable 
data, but they must be interpreted in relation to other physical 
signs. Such observations alone do not furnish us with a basis for 
treatment any more than they, unaided, permit us to make a diag- 
nosis. In this respect a sphygmomanometer is like a thermometer 
— its readings must be construed in the light of other findings. 
We have seen cases exhibiting a practically normal systolic and 
diastolic pressure associated with dyspnea, cyanosis, and edema, 
showing that the blood-flow was not normal. 

Observations of the systolic pressure alone are of relatively little 
value. They indicate, it is true, the strain to which the arteries 
are subjected, but the diastolic pressure, the variations of which 
correspond more or less closely to those of the mean pressure, is 
the real indication of the work the heart has to do. Systolic pressure 
may suddenly vary greatly from many diverse causes — fright, 
excitement, etc. — but the diastolic pressure is a much less easily 
disturbed factor, and may hence be a valuable criterion in deciding 
whether organic, vascular or cardiac changes are present. Since 
the diastolic pressure can now be readily, quickly and accurately 
determined by observing the appearance of the fourth auscultatory 
phase, there can no longer be any excuse for neglecting this far wore 
important of the two phases of arterial tension. ^Ye have already 
learned in most conditions to attribute more importance to the 
diastolic than to systolic readings. 

Pulse Pressure. — The difference between the systolic and the 
diastolic pressure roughly indicates the volume of the pulse. 
From a study of pulse pressure certain deductions can often be 
drawn, but it must be remembered that these are not absolute 
nor always trustworthy criteria. 1 





Systolic 


Diastolic 


Fulse 




pressure. 


pressure. 


pressure 


Increased peripheral resistance 


+ 


+ + 


— 


Decreased peripheral resistance 


— 





+ 


Increased heart rate .... 


+ 


+ + 


— 


Decreased heart rate .... 


— 





+ 


Increased systolic discharge 


. + + 


+ 


+ 


Decreased systolic discharge . 





- 


— 



1 Wiggers, C. J., Modern Aspects of the Circulation in Health and Disease. 
Phila., 1915, p. OS. 



EXTREMES OF PRESSURE COMPATIBLE WITH LIFE 131 

The diastolic pressure is normally about three-fourths of the 
systolic pressure and the pulse pressure, one-quarter of the systolic 
pressure. A pulse pressure persistently as low as 20 or as high as 
GO mm. is definitely pathological. 

A high systolic with a normal diastolic -pressure may result from 
emotional disturbances and as a result of physical exertion. 

A low systolic with a high diastolic -pressure often indicates myo- 
cardial weakness in association with severe pressor factors such as 
nephritis or vascular spasm. 

A low systolic and diastolic pressure occurring in a person who 
is up and about (essential hypotension), while it does not necessarily 
imply a poor circulation, is definitely associated with diminished 
reserve force — "staying power." 

A high systolic with a low diastolic pressure is most characteris- 
tically seen in aortic insufficiency; it may, however, result from 
peripheral vascular dilatation associated with forcible heart action. 

THE EXTREMES OF PRESSURE COMPATIBLE WITH LIFE. 

Hypertension. — Systolic blood-pressures above 235 mm. are 
unusual and above 250 mm. are rare. Hirst has reported a recovery 
in puerperal eclampsia with a pressure of 420 mm. Hg. Needless 
to say, such a pressure could not long be maintained without some- 
thing giving out. Many patients live for years with pressures 
ranging about 200 systolic and 120 diastolic, and occasionally such 
pressures are compatible with hard manual labor, 1 but a sudden 
termination in these cases is always a possibility. Strauss's patient 
lived for five years with a systolic pressure between 260 and 270 mm. 
Cook and Briggs reported 400 mm. in a case of cerebral hemorrhage. 

Hypotension. — A systolic pressure of 105 is common among many 
essential hypotension cases which are up and about. Not many 
are able to do so, however, if the systolic pressure falls below 100 
or the diastolic below 50. Rolleston has reported a remarkable 
case of a man with a lingual carcinoma, who lived for several 
weeks with systolic and diastolic pressures of 70 and 35 respectively. 
Agonal systolic pressures of 40 mm. have been reported and 60 
mm. probably represents the lowest figure at which the coronary 
and medullary circulation can be kept up, even for a short time. 
Some of the earlier figures, such as those of John, of 35 to 40 in 

1 McCurdy, S. M., Physical Examination and Regeneration of Employees, Jour. 
Amer. Med. Assn., 1915, lxv, 2050. 



132 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

a case of advanced tuberculosis, are open to question on account 
of faulty instrumentation. Janeway has seen systolic pressures of 
40 mm. as transient phenomena during surgical operations. 

All clinical blood-pressure estimations must be accepted only as 
approximately correct. In addition to the fact that the determi- 
nation of the diastolic pressure presents certain difficulties we are 
confronted with the fact that, even if this could be accurately 
measured, we would still be only measuring the blood-pressure of 
the brachial artery. Living vessels possess a distinct tonus — the 
ability to contract and to dilate — the amount of which in a given 
case we are thus far unable to determine. In addition to this 
we must bear in mind that the blood-pressure mechanism is an 
extremely labile one which is subject to frequent fluctuations, due 
to many different causes. 

On the other hand, thousands of blood-pressure measurements 
on different individuals have shown that pressure relations are 
fairly constant under similar circumstances; that there are definite 
and distinct bounds beyond which normal variations do not extend, 
and again that there are certain abnormal values which, if constantly 
found in a given individual, point very definitely to well-established 
pathological conditions. 

THE CHOICE OF AN INSTRUMENT. 

For general office work some instrument of the Riva-Rocci type 
is unquestionably to be preferred. Of this type of instrument a 
great many different models have been placed on the market. 
Although varying in detail of construction they are all based on 
the same principle. Good results may be obtained with most of 
them. On the whole, the last model of Nicholson's sphygmo- 
manometer is the most satisfactory instrument to be obtained, 
being compact, readily portable and yet possessing the advantages 
of the mercury manometer. 

In the personal choice of an instrument we should be governed 
by a number of factors, i. e.: (1) Accurate standardization. (2 
General workmanship. The instrument should be made of flint 
glass, as the lead in American glass reacts with the mercury. In 
the same way the mercury will form an alloy if allowed to come in 
contact with any metals save steel and platinum, producing tur- 
bidity and increasing friction. It is also affected by rubber, owing 
to the sulphur which this substance contains. All joints must of 



CLASSIFICATION OF BLOOD-PRESSURE INSTRUMENTS 133 

course be tight. It is essential for accuracy that the cuff have a 
width of 12 cm. and that the canvas or leather backing be suffi- 
ciently rigid to maintain the width of the aforesaid rubber portion. 
(3) Compactness and portability — including the ease and celerity 
with which the instrument can be set up for use, the devices 
employed to prevent the spilling of the mercury when in transit, 
and the bulk of the apparatus "when taken down. (4) The ampli- 
tude of the pulsation transmitted to the mercurial column. If the 
auscultatory method of blood-pressure reading be employed, the 
amount of visual oscillation obtainable loses its importance, and 
satisfactory results may be obtained with any accurate manometer 
if fitted with a proper cuff. 

Compressed-air manometers are small and accurate (since the 
stopcock when open equalizes barometric and temperature varia- 
tions). The adjustment of the drop used as an indicator is some- 
times troublesome. Aneroid instruments for bedside use, owing 
to their small size and ready transportability, have much to com- 
mend them. When well made they may not require adjustment 
for considerable intervals, although comparisons with a mercury 
manometer must from time to time be made. 

Spring manometers require frequent standardization, without 
which procedure inaccuracies may result. The von Recklinghausen 
apparatus is somewhat bulky and is based on c.c. H 2 0, which 
standard has not been widely adopted. 

The kind of pump selected is of minor importance. The rubber 
bulb is light but less durable than the heavier metal variety. The 
von Recklinghausen bicycle-pump type is both heavy and bulky, 
but one or two strokes suffice for inflation. Compressed-air tanks, 
such as are currently used in rhinological work, may be used when 
rapid inflation of the cuff is desired. Errors due to stasis may 
thus be minimized. 

CLASSIFICATION OF BLOOD-PRESSURE INSTRUMENTS. 

I. Mercury manometers: 

1. Reservoir: Riva-Rocci, Cooke, Stanton, Nicholson, Hill, 

Kercher, Hollman, Gartner, Westenrijk. 

2. U-shaped; Janeway, Faught, Martin, Linnell, Fellner, 

Hamilton, Schneider, Beachler, Brown. 
II. Compressed-air manometers: Oliver, Bendick, Herz. 
III. Aneroid manometers: Rogers, Brunton, Tycos, Faught, 
Pachon, Jacquet, McKeson, Bristol. 



134 THE INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

IV. Spring manometers : von Recklinghausen. 
V. Instruments for graphic registration: Erlanger, Gibson, 
Bingel, Singer, Uskoff, Silbermann, Brugsch, Stursberg, 
Muenzer, Strauss-Fleischer, Bussenius, Wybauw. 

VI. Instruments consisting of or which may be fitted with 
special oscillating indices, such as the Fedde or Pal oscil- 
lometers, Bing, Nicholson, Vaquez, Faught, Widmer. 



CHAPTER IV. 
VENOUS BLOOD-PRESSURE. 

By J. HAROLD AUSTIN, M.D. 

Various methods of determining venous blood-pressure in man 
have been devised. They may be grouped into five types: 

I. Gartner's Phenomenon. — Gartner, 1 in 1902, contended that if 
the left arm is slowly raised, the veins at the elbow which become 
distended when the arm is dependent will suddenly collapse upon 
reaching a certain level. He assumed that the elevation at this point 
above the level of the right auricle is a measure in centimeters of 
blood of the pressure at the right auricle. It is to be remembered 
that 10 cm. of blood equals 10.6 cm. of water. As the level of the 
heart Gartner took the junction of the upper border of the left fifth 
costal cartilage with the sternum. Oliver 2 used the same method 
but observed the veins on the dorsum of the hand. Prym, 3 however, 
showed that Gartner's phenomenon occurs at different levels 
when the arm is raised at different rates, and that, moreover, the 
veins have a tonus of their own which may be stimulated by cold 
or by stroking, and this tends to accelerate their collapse. Meinertz 4 
has noted that exercise of one arm frequently raises the level at 
which the veins collapse in that arm without affecting the level 
in the other arm. The state of the circulation and vascular tonus 
locally, as well as the pressure in the right auricle, therefore influence 
Gartner's phenomenon. 

II. Spring Manometers. — In 1898 Oliver 5 attempted to measure 
venous pressure by means of a spring-pressure manometer. A 
button attached to the spring of the manometer was pressed against 
one of the larger veins of the arm with sufficient force to obstruct 
the flow. The vein for an inch or so proximal to this point was 
then stripped by the finger. The pressure against the vein by the 

1 Munch, med. Woch., 1904, lxxiv, 2038. 

2 Quar. Jour. Med., Oxford, 1907-08, i, 59. 

3 Munch, med. Woch., 1904, li, 60. 

4 Ztschr. f. exper. Pathol, und Therap., 1908. 
6 Jour. Physiol., 1898, xxii, li; 1898, xxiii, v. 



136 



VENOUS BLOOD-PRESSURE 



manometer was then gradually reduced and at the moment the 
emptied section of vein began to fill, the pressure recorded by the 
manometer was noted. This was believed to equal the venous 
pressure at that point. Subsequently both Frey 1 and Sewall 2 
independently devised similar spring manometers. 




Fig. G5. — Hooker's venous pressure apparatus. A small glass chamber (B) measur- 
ing 1 by 2 cm. is held temporarily by a rubber band over a suitable vein on the back 
of the hand, as shown at A. A rim of collodion is applied and in drying it seals 
the chamber to the skin. The rubber band is then removed and the chamber con- 
nected by a rubber tube to the water manometer M. By pressing on the man- 
ometer bulb C the air pressure in the chamber is raised and a reading is made "at 
the point where slight oscillations of pressure cause the vein shadow to come and go 
promptly just before the vessel is completely collapsed." This pressure is recorded 
directly by the water manometer. The hand is held at the level of the midpoint of 
the anteroposterior diameter of the body at the costal angle. 



III. Pressure Chambers over the Vein (Fig. 65).- — In 1904 von 
Basch 3 attempted to measure venous pressure by placing a small 

1 Deutsch. Archiv f. klin. Med., 1902, lxxiii, 511. 

2 Jour. Amer. Med. Assn., 190G, xlvii, 1279; Trans. Assoc. Amer. Phys., Philadel- 
phia, 190G, xxi, 20. 

3 Wien. klin. Rundschau, 1900, pp. 549 and 572. 



DOUBLE-CUFF MANOMETERS 137 

glass cylinder over the vein, and raising the air pressure in the 
cylinder until the vein collapsed or releasing the air until the vein 
refilled. This method was improved upon by von Recklinghausen,' 
and later by Hooker and Eyster, 2 so as to reduce the error caused 
by pressure of the wall of the cylinder against the vein. The latter 
authors compared readings made with a manometer in the facial 
vein of a dog with those made with their instrument over the neigh- 
boring exposed external jugular. The pressure was artificially 
altered by tilting the animal's body. The results follow: 



Observation. 


Manometer in facial vein. 


Pressure chamber over external jugular 


1 . . 


. . 4.5 cm. HzO 


4.0 cm. H2O 


2 . . 


. . 10.0 cm. H 2 


10.0 cm. H,0 


3 . . 


. . 13.0 cm. H2O 


14.0 cm. H2O 


4 . . 


. . 5.0 cm. H2O 


5 . cm. H2O • 



A fuither improvement of this instrument has been made by 
Hooker, 3 and in its present form the instrument has proved most 
satisfactory. Two conditions are necessary for its use: First, that 
the vein shall stand out sufficiently from the surrounding skin 
level to give a distinct shadow by oblique illumination and, second, 
that the vein wall must be collapsible. Hence "old patients with 
phlebosclerosis, patients with exceedingly edematous or fat hands, 
and patients with continuously small veins are not satisfactory 
for this method" (Clark). 

IV. Double-cuff Manometers (Fig. 6G). — In 1912 two instruments 
upon the same principle were introduced independently, one by 
L. Frank and M. Reh 4 and the other by A. A. Howell. 5 The instru- 
ments consist of two cuffs, each attached to a water manometer. 
One cuff is applied to the upper arm, the other to the forearm. 
The forearm cuff is inflated so as to fit against the arm snugly 
without exerting, however, more than 1 cm. (Frank and Reh) to 
3 cm. (Howell) H2O pressure. The upper cuff is then slowly inflated 
until the water in the forearm manometer is seen to be rising. This 
rise is assumed to be evidence that the venous flow beneath the 
upper cuff has been obstructed and that the blood, being dammed 
back, has increased the volume of the forearm with consequent 
displacement of air from the lower cuff and a rise of water in its 

1 Arch. f. exper. Path, und Pharm., 1906, lv, 463. 

2 Johns Hopkins Hosp. Bull., 1908, xix, 274. 

3 Amer. Jour, of Physiol., 1914, xxxv, 73. 

4 Zeitsch. f. exper. Path, und Therap., Berlin, 1912, x, 241. 
'Arch. Int. Med., Chicago, 1912, ix, 148. 



138 



VENOUS BLOOD-PRESSURE 



attached manometer. The forearm cuff and its manometer are 
used, therefore, as a sort of plethysmograph. It is further assumed 
that the blood-flow beneath the upper cuff is first obstructed when 
the pressure in this cuff equals the venous pressure. The instrument 
of Frank and Reh differs from Howell in that it provides for graphic 
registration of the readings. Reference to the table on p. 141 
shows that Howell's figures are somewhat higher than those of 
Frank and Reh, which may be in part explained by the higher 
pressure used by Howell in his plethysmographic cuff. 



D \I\ 




Fig. 66. — Howell's venous pressure apparatus. Upper and lower cuffs applied 
and attached to their respective water columns. E, light cuff for constricting upper 
arm and obstructing venous return; F, glass T and bulb, by means of which pressure 
is raised in E; G, water column measuring pressure in E; B, inelastic covering of 
light material encircling rubber bag; C, glass T, side tube, and clip, by means of which 
pressure can be raised; D, water column measuring pressure. 



V. Intravenous Needle. — In 1909-10 Moritz and von Tabora 1 
published studies of venous pressure measured by the pressure 
required to cause normal saline to enter the median vein at the level 
of the heart. The method was to place the patient in the recumbent 
position, and then introduce into the median vein with the usual 
precautions a needle connected with a burette of normal saline. 
The saline was allowed to enter the vein, its level in the burette 
falling until further flow ceased. The level of the saline above the 

1 Deutsch. Arch. f. klin. Med., 1909-10, xcviii, 475. 



INTRAVENOUS NEEDLE 



139 



heart was then read, and the resulting figure was assumed to be the 
venous pressure at the heart in centimeters normal saline, which 
since 10 cm. normal saline equals 10.07 cm. H 2 may be reckoned 
as cm. H 2 0. In all the other methods described the patient is 
in sitting posture, and the level of the heart is by most observers 




Fig. 67. — The Moritz-Tabora venous blood-pressure apparatus: A, cannula in vein; 
B, manometer scale; C, level; D, escapement. (After Hoffmann.) 



taken according to von Recklinghausen's rule as at the level of 
the apex of the subcostal angle. With the patient recumbent, 
Moritz and von Tabora assume the heart level to be that of a 
point on the fourth rib 5 cm. below the level of the anterior thoracic 
surface. This method of measuring venous pressure is the most 
accurate of those described for use in man. 



140 VENOUS BLOOD-PRESSURE 

Capillary Pressure. — In 1875 the attempt to measure capillary 
pressure was first made by von Kries. 1 A small glass plate of 
known area was laid upon the skin or mucous membrane and 
pressure was exerted evenly upon it by means of delicate weights. 
The amount of weight required to produce a just perceptible 
pallor of the skin or mucous membrane was taken to be the capillary 
pressure, and the weight and area over which it acted being known, 
the pressure per unit of area and hence the pressure in mm. Hg. 
(1 mm. Hg = 0.0136 gm. per sq. mm.) or in cm. H 2 (1 cm. H 2 
= 0.01 gm. per sq. mm.) can be calculated. Von Basch and von 
Recklinghausen measured capillary pressure with the same appara- 
tus employed for measuring venous pressure by applying it over 
a skin area, the former noting the pressure required to just cause 
complete blanching, the latter raising the pressure above the point 
required to produce complete pallor, and on gradually lowering the 
pressure noting the moment when flushing first became apparent 
and also when flushing became complete. 

Lombard 2 has recently developed a refinement of these methods. 
He finds that if the skin be wet with glycerin or with a transparent 
oil, by the use of a low-power magnification (from 10 to 35 diameters) , 
and either bright daylight or a Nernst lamp, the papilla 3 of the 
skin with their superficial bloodvessels are rendered visible. He 
applies this method either with a weighted glass plate according 
to von Kries, or with a specially constructed chamber similar in 
general principle to von Recklinghausen's. Lombard's chamber 
consists of an inverted truncated cone. The smaller end, which 
fits against the skin, has a diameter of 24 mm., its walls are 3 mm. 
thick, and the pressure is therefore applied over a circular area 
of 18 mm. in diameter. Over the periphery of this area the skin is 
covered by a rubber dam, which aids in preventing leakage between 
the chamber and skin. A central circular area 5 mm. in diameter 
is left open for inspection through the microscope. In using the 
von Kries plate, Lombard has found the optimum dimension for 
his purposes to be 1 mm. square. If larger plates be used, the 
weight is borne disproportionately at the edges. Lombard has 
shown, as may be seen in the following table, great variation in 
pressure in capillaries of different sizes. The measurement of 
capillary pressure in individuals or in pathological conditions can 
hardly be of value, therefore, while we lack means of discriminating 

1 Berichte ii. d. Verhandlung der koniglich sachsisch. Gesellsehaft d. Wissen- 
schaften z. Leipsic math. Phys., 1875, clxxvii, 147. 

2 Amor. Jour. Phys., 1912, xxix, 335. 



VARIOUS FACTORS INFLUENCING VENOUS PRESSURE 141 

between the particular type of capillary under consideration. 
Inspection of the table suggests that the grosser methods of von 
Kries, von Basch, and von Recklinghausen measure the pressure 
in the medium-sized and larger capillaries on the arterial side. 

Table I. 

Level <>f heart - 
Capillary pressure. Cm. HsO Mm. lie 

von Kries, finger, Grst pallor 51.3 37.7 

von Basch, hand, complete pallor 34 to 41 25 to 30 

von Recklinghausen, hand, first flush .... 93 to 99 68 to 72.5 

von Recklinghausen, hand, complete flush . 75 55 1 

Lombard — Largest capillaries 82 to 95 CO to 70 

Medium capillaries . . . .' . . 48 to 61 35 to 45 

Smallest capillaries, hack of hand . . 20.0 to 30.9 15. 1 to 22.7 

Smallest capillaries, finger nail . . 23.3 to 37.5 17.1 to 27.6 

Most superficial and smallest veins . 20.5 to 27 15 to 20 

Suhpapillary venous plexus . . 13.5 to 20.5 10 to 15 

Table II. 
At level of heart. Normal. Pathologic. 

Venous pressure. Cm. H2O Mm. Hs;. Cm. H2O Mm. Hg. 

Sewell 4.6 to 5.2 3.4 to 3.8 

von Basch .... 8.8 6.5 

von Recklinghausen: filled 14 to 22 

empty . 20 to 26 

Hooker-Eyster . . . 3 to 10 2 . 2 to 7 . 3 

av. 8 av. 5.9 

Frank and Reh . . . 1 to 6 0.7 to 4.4 to 17 to 12.5 

Howell 4 to 13 2.9 to 9.5 7 to 25 5.1tol8.4 

av. 7.6 av. 5.6 av. 13.9 av. 10.2 

Moritz and Tabora . . 1.1 to 8.7 0.8to6.4 

av. 5.2 av. 3.8 

Summary 1 to 13 0.7 to 9.5 up to 25 up to 18 + 

VARIOUS FACTORS INFLUENCING VENOUS PRESSURE. 

The position of a part with relation to the heart is probably the 
most important factor in determining venous pressure. The weight 
of the blood is such that the pressure of one inch of blood is approxi- 
mately equal to 1.9 mm. Hg. or 2.6 cm. H2O. It has been shown, 
however, by von Recklinghausen that the veins of the feet do not 
actually exhibit the pressure demanded by calculation upon this 
basis. This is shown in the following table: 

Venous Pressure at Various Levels. 
(Data from von Recklinghausen.) 
Distance 
below heart In cm. H2O In mm. Hg. 

in inches. calculated. Measured. calculated. Measured. 

Heart 10 .. 7.3 

Symphysis pubis, 
subject sitting 

or standing. . 12 inches 42 . , 31 

Foot, subject 

sitting ... 34 " 102 55 to 80 75 40 to 59 

Foot, subject 

standing . . 48 " 140 79 to 100 103 58 to 73 

Foot, subject 
recumbent. . 10 8 to 10 7.3 5.9 to 7.3 



142 VENOUS BLOOD-PRESSURE 

This discrepancy von Recklinghausen supposes to be due to 
the action of the muscle masses of the extremities which, by their 
intermittent pressure upon the veins, aided by the action of the 
valves of the veins, serve to propel the blood up into the vena cava, 
where he supposes the venous pressure actually exhibits its cal- 
culated value. This importance of muscular activity in promoting 
the return of venous blood from the extremities may explain in 
part the discomfort incident to prolonged standing in one position. 
The importance of position in the determination of venous pressure 
is further shown by the fact that raising one arm above the level 
of the head increases the venous pressure in the opposite arm. 

Barach and Marks 1 have noted that readings of venous pressure 
in the arm do not always show a constant relative difference 
proportional to the elevation or depression above or below the 
level of the right auricle. Hence venous pressure should be meas- 
ured at the level of the right auricle rather than at another level 
followed by correction to the level of the auricle. 

Changes in arterial pressure do not readily alter the venous press- 
ure, and the capillary pressure, at least of the smaller capillaries, 
is much more dependent upon venous than upon arterial pressure. 
Hooker finds that there is no relation between venous pressure and 
changes in pulse rate, and that local changes in vascular tone (cold, 
heat, etc.) do not alter the venous pressure in the hand. Burton- 
Opitz 2 was able to show only a very slight fall of venous pressure 
in the external jugular of a. dog upon occluding a portion of the 
arterial supply to the head. 

Normal venous pressure at the level of the right auricle was found 
by Barach and Marks to range in the erect posture between 8 and 
18 cm. H 2 and in the recumbent posture between 3.5 and 11 cm. 
H 2 0. Muscular exertion either general or local was found by 
Hooker and Wolfsohn, 3 Elfers 4 and Schott, 5 to increase the venous 
pressure from a slight rise up to 14 cm. H 2 0. Hooker 6 has noted 
a distinct diurnal variation under normal conditions of health even 
in individuals confined to bed. He observes a gradual rise through- 
out the day from 10 to 20 cm. H 2 to an average diurnal pressure 
of 15 cm. and a fall during sleep to as low as 7 to 8 cm. During 

i Arch. Int. Med., 1913, xi, 485. 

= Amer. Jour. Physiol., 1903, ix, 198. 

3 Amer. Jour. Physiol., 1909-10, xxv, 24; 1911, xxviii, 235. 

4 Inaug. Diss., Kiel, 1911. 

6 Deutsch. Arch. f. klin. Med., 1912, cviii, 537. 

6 Amer. Jour. Physiol., 1914, xxxv, 73. 



VARIOUS FACTORS INFLUENCING VENOUS PRESSURE 143 

sleep he lias noted a venous pulse of peripheral origin in the veins 
of the hands. Clark 1 found in 4 bed patients without cardiac 
complications, a diurnal variation of from 8 to 10 cm. H 2 0, the 
maximum (10-10 cm.) being reached from 2 to 8 p.m., and the 
minimum (5-8 cm.) between 10 p.m. and 6 a.m. This author from 
repeated observation on 14 cases, 6 with decompensation, 8 with 
good compensation, concludes that a venous pressure above twenty 
is pathological. In cardiac cases, the diurnal variation was found 
by Clark to be reversed, the highest pressure occurring during the 
sleeping hours. Venous pressure continuously above 20 cm. which 
was not lowered by digitalis, was an indication of grave cardiac 
involvement. On the other hand, with a venous pressure below 
20 cm. no definite change in the pressure was observed from digitalis 
therapy. The venous pressure and the urinary output generally 
showed a significant inverse variation in cases of cardiac decom- 
pensation. Aspiration of pleural fluid and venesection both lowered 
venous pressure as a rule in his series, but after the latter procedure 
the subsequent rise of venous pressure was rapid. 

Respiration. — Burton-Opitz made careful studies of the effect 
of respiration upon the venous pressure in the external jugular of 
a dog, and found that with expiration the jugular pressure rose 
and that during the pause following expiration it began to fall and 
continued to fall throughout the early part of inspiration, a curve 
similar, therefore, to that of the arterial pressure in the respiratory 
phases. Upon expiration the intrathoracic pressure rises and the 
venous blood does not readily enter the thorax, but being dammed 
back causes rise of peripheral venous pressure. Upon inspiration 
the intrathoracic pressure falls and the venous blood flows readily 
into the thorax, with fall in the peripheral venous pressure; near 
the thorax the venous pressure may be negative during inspiration. 
The respiratory variation found in the external jugular pressure 
is as much as 3.8 cm. H 2 0, and becomes greater as the thorax is 
approached. The opening of the thorax by increasing the intra- 
thoracic pressure (which is normally less than the atmospheric) 
causes a prompt rise of venous pressure of from 1.5 to 3.5 cm. H 2 0. 

Cardiac Action. — Impaired cardiac action by leading to venous 
stasis produces an increase of venous pressure. Experimentally, 
stimulation of the peripheral end of the sectioned vagus produces 
a slight rise of venous pressure. Clinically, any form of myocardial 

1 Arch. Int. Med., 1915, xvi, 587. 



144 VENOUS BLOOD-PRESSURE 

decompensation leads to increase of venous pressure which may 
rise to 30 cm. H2O in the veins of the arm at the cardiac level. 
Indeed, increased venous pressure may, in the early stages, be the 
only sign of circulating stasis. 

Intravenous Injection. — That intravenous injections increase the 
venous pressure more proportionately than they do the arterial 
was shown by Bayliss and Starling. 1 Rise of venous pressure at the 
heart also results from abdominal pressure, bandaging or elevation 
of the extremities, or from elevation of the abdomen above the 
level of the heart. The importance of venous pressure in relation 
to cardiac output has already been discussed. Experimentally 
as a result of therapeusis, a rise of venous pressure occurs after large 
doses of epinephrin, pituitrin, and alcohol, not after digitalis, 
strophanthin, strychnin or caffein. This rise is proportionate to, 
and apparently the result of disturbed heart action. It is therefore 
apparently simply a stasis reaction and not the result of vasomotor 
influence. A fall of venous pressure may follow the administration 
of the nitrites or large doses of morphin, and since cardiac func- 
tionation remains unimpaired, may be attributed to a direct 
influence on the vasomotor mechanism. 2 

1 Jour. Physiol., 1894, xvi, 159. 

2 Capps, J. A., and Mathews, S. A., Venous Blood Pressuie as Influenced by the 
Drugs Used in Cardiovascular Therapy, Jour. Am. Med. Assn., 1913, lxi. 388. 



CHAPTER V. 

THE FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

AS DETERMINABLE BY BLOOD-PRESSURE 

ESTIMATION AND ALLIED TESTS. 

In the following chapter are described a number of methods 
which have been suggested in the hope of throwing more light on 
the question of the functional efficiency of the circulation. Most 
of them are based on sound theoretic principles, and would be 
invaluable if our instrumental measurements were sufficiently 
exact and comprehensive to insure an accurate basis for our deduc- 
tions. Unfortunately, however, the data obtainable by sphygmo- 
manometry, etc., are, even when collated with the greatest care, 
subject to unavoidable sources of error, and hence our results are 
only approximate. To use such data as a basis for elaborate calcula- 
tions, entailing the use of involved mathematic and algebraic 
formulae for the elucidation of the complex factors included in the 
static and dynamic laws of the circulation, only magnifies our errors 
and often leads to a veritable reductio ad absurdum. Thus far it 
must be admitted no entirely satisfactory method has been perfected, 
mainly because we cannot measure vascular tonus, or estimate 
the role of psychic processes. Furthermore, to yield definite 
indications many of the tests have to be carried to a point at 
which concomitant symptoms and ordinary physical signs are of 
themselves sufficiently evident criteria of functional insufficiency. 
Unquestionably, however, some of the methods about to be de- 
scribed do throw a useful light on the problem under consideration, 
especially if the results thus obtained are accepted with due reserve. 

Many are the attempts which have been made and numerous 
the methods suggested for determining the functional capacity 
of the heart. The importance of this subject from a diagnostic, 
prognostic, and therapeutic stand-point cannot be overestimated. 
Such procedures as are based in part, at least, upon blood-pressure 
measurements will be here considered. 

Generally speaking, such tests depend upon the way in which 
10 



14b' FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

the pulse rate and blood-pressure both respond — quantitatively, 
qualitatively, and temporarily — to definite amounts of muscular 
exertion or to change of posture (see p. 48). This subject has been 
extensively studied by Masing, Buttermann, Christ, Staehelin, 
and others. 1 The work performed was either definitely measured 
with various forms of apparatus, or roughly estimated by such 
tasks as lifting, stair-climbing, walking, etc. 

"In blood-pressure and exercise we have an unfailing guide to 
the true condition. Whatever the abnormality the great question 
is the integrity of the heart muscle, the reserve force of the heart, 
for upon this chiefly depends the prognosis. The pulse should be 
counted, the heart examined, and the blood-pressure taken, and 
then with the cuff attached to the arm, the applicant should be 
exercised to the equivalent of climbing two flights of stairs and 
then reexamined quickly. Exercise when not too severe will 
regulate the pulse if the condition is simple. If serious disease is 
present the irregularity will be greatly increased. - If the heart 
muscle is in prime condition the systolic pressure will jump 15 to 
40 mm. and, tested every two minutes, will, be found to resume 
its original place in six or eight minutes. If the condition is bad, 
in a powerful effort of the heart to respond, the rise may be even 
greater, but the return will be exceedingly slow, sometimes requiring 
20 or 30 minutes. If the state of the muscle is extremely bad and 
the reserve force exhausted, the systolic pressure may fall instead of 
rising and the diastolic remain stationary, or rise a little, creating 
a very small pulse pressure. It will be a long time before graphic 
instrument tracings are required in life insurance, if ever, but we 
have in exercise and blood-pressure a thoroughly reliable test, and 
it is the duty of the examiner to be safe in his recommendation of 
every applicant." 2 

Crampton's Test of Vasomotor Efficiency. — In rising from the 
recumbent to the erect posture blood-pressure tends to fall as a 
result of gravity. Unless this tendency were automatically regu- 
lated, syncope would occur as a result of cerebral anemia. In a 
normal vigorous man, however, such a change of position causes a 
rise of blood-pressure amounting to 8 or 10 mm. Hg. This increase 
may result from increased vasomotor tone or from increased cardiac 
work, or as a result of both factors. Bearing these facts in mind 

1 For bibliography, see Norris, G. W., The Functional Capacity of the Heart, 
International Clinics, 1907, 17th series, vol. i. 

2 Lankford, J. S., The Heart in Life Insurance, Med. Rec, October 17, 1914, p. 687. 






CRAMPTON'S TEST OF VASOMOTOR EFFICIENCY 147 

Crampton 1 has devised the following table to test vasomotor effi- 
eieuey through the observation of pulse rate and blood-pressure 
responses to postural change. The tables while setting what is 
perhaps a high normal have shown that vasomotor tone in the same 
individual varies greatly as a result of mental or physical fatigue, 
infectious processes, etc. It may be used with especial edification 
in the study of essential hypotension cases. 

The Technic. — "The sphygmomanometer is adjusted over the 
brachial artery and the patient is placed on a comfortable couch 
with a low pillow. The heart rate is counted by quarter-minutes 
and a gradually descreasing rate is usually observed. Counting 
should continue until two successive quarter-minutes are the same, 
this is multiplied by 4 and recorded. The systolic pressure is 
then taken preferably by auscultation. The patient stands, the 
heart rate is counted as before until it reaches the 'standing nor- 
mal,' when it is recorded, and the blood-pressure is then taken. 
The differences are calculated and reference is made to the scale. 

"For example — Case XX: L. V., age seventeen years, said to be 
in good condition at 1 1 : 20 a.m. 

Pulse rate. Blood pressure. 

Horizontal 68 100 

Vertical 104 94 

Difference +36 -6 

Percentage record, 20. 

"This is a very poor record taken from an apparently normal, 
strong young football player of exceptional ability who had pre- 
viously given records above 80. 

"I was at a loss to account for this, for questioning failed to bring 
out any history of loss of sleep, dissipation, or illness. He looked 
quite as 'fit' as usual. He was absent next day, and remained 
home for a week with a 'cold and fever.' It is evident that the 
test revealed a weakened vasotone, the beginning of actual illness 
before any other symptom could be noted. Others who have used 
this test have noted similar cases." 

If the vasomotor tone is deficient, the heart must make up for it 
by an increase in rate — the greater the increase, the less efficient 
the vasomotor tone. 

"The usual range of the systolic pressure is from +10 to —10 
of the heart rate increase from to 44, as observed from records of 
a large number of cases. Upon a statistical balancing of these two 

1 Blood Ptosis, New York Med. Jour., November 8, 1913. 



148 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

series of frequencies, and assigning equal percentages to equal 
ranges, the following scale is constructed: 

PERCENTAGE SCALE. 

Vasomotor Tone. 
Blood-pressure. 



Heart rate • 

increase. +10 


+s 


Increase 

+6 +4 


+2 





-2 


-4 


Decrease 

-6 -8 


-10 


to 4 . .100 


95 


90 


85 


80 


75 


70 


65 


60 


55 


50 


5 to 8 








95 


90 


85 


80 


75 


70 


65 


60 


55 


50 


45 


9 to 12 








90 


85 


80 


75 


70 


65 


60 


55 


50 


45 


40 


13 to 16 








85 


80 


75 


70 


65 


60 


55 


50 


45 


40 


35 


17 to 20 








80 


75 


70 


65 


60 


55 


50 


45 


40 


35 


30 


21 to 24 








75 


70 


65 


60 


55 


50 


45 


40 


35 


30 


25 


25 to 28 








70 


65 


60 


55 


50 


45 


40 


35 


30 


25 


20 


29 to 32 








65 


60 


55 


50 


45 


40 


35 


30 


25 


20 


15 


33 to 36 








60 


55 


50 


45 


40 


35 


30 


25 


20 


15 


10 


37 to 40 








55 


50 


45 


40 


35 


30 


25 


20 


15 


10 


5 


41 to 44 








50 


45 


40 


35 


30 


25 


20 


15 


10 


5 






Note. — In case of increase in pressure higher than +10 add 5 per cent, to the 
+10 column for each 2 millimeters in excess of 10. 

"This scale provides a convenient and intelligible method of 
recording and reporting cases and permits a numerical statement 
of the function in question. Its 100 mark indicates a perfectly 
efficient working of the vasomotor system under test, the zero is 
approximately the point where the average person is unable to 
maintain the erect posture." 

Among 116 athletes R. Tait McKenzie found the postural change 
in pulse rate and systolic blood-pressure average as follows: 

Number of Pulse. Blood-pressure, 

students. Lying. Standing. Lying. Standing. 

34 78 86 114 113 

28 75 85 120 121 

30 83 85 120 114 

24 70 79 110 114 

116 77 84 116 115 



It will be noted that there was a very constant variation in the 
pulse rate amounting to about seven beats per minute between 
the two postures. The blood-pressure findings were much more 
variable and when an average was established they were practically 
identical in the two positions. Among 388 students with cardiac 
abnormalities — arhythmia, murmurs, etc., the systolic blood- 
pressure average was somewhat higher (138+ mm. Hg.) than 
among the athletes with normal hearts. 



CRAMPTON'S TEST OF VASOMOTOR EFFICIENCY 149 

Passive change of posture. 

"When the element of muscular effort has been eliminated, 
change of bodily posture from the erect to the horizontal will cause 
an increase in the maximum pressure, a decrease in the minimum 
pressure, and an increase in the pulse pressure. After five minutes 
in the horizontal posture when the subject is retilted to the erect 
posture, the maximum pressure will diminish, the minimum pressure 
increase and the pulse pressure diminish. It will be noted that in 
both instances the pulse pressure follows the same trend as the 
maximum pressure. Change of posture from the erect to the hori- 
zontal causes a fall in the venous pressure. Change of posture 
from the horizontal to erect causes an increase of the venous 
pressure." 1 

During muscular exercise we see an increased respiratory gas 
interchange, the amount of which may exceed that occurring during 
rest over twentyfold. Associated with this there is a marked 
increase in the rate of blood-flow, so that the normal circulation, 
the time of which is fifty-five seconds, may be reduced to five 
seconds during exercise. Such changes must, of course, produce 
enormous alterations in blood-pressure values. 

Muscular exertion may be accompanied either by a fall or by a 
rise of pressure, and it has been found that the more fit and well- 
trained the animal the less the tendency for the pressure to rise. 
Thus in horses and in well-trained athletes there is a fall. The 
average man shows a primary rise, followed by a fall upon cessation 
of work. The more strenuous the work and the less trained the man, 
the greater and the earlier will be the fall. This may result from 
cardiac weakness or may be a result of Nature's safeguard against 
cardiac overstrain, the fall of pressure being brought about reflexly 
through the agency of the depressor nerve. During youth both 
pulse and blood-pressure are more labile during exercise and tend 
to keep pace with each other. In adults there is less tendency for 
the pulse and more for the pressure to rise. In health both pulse 
and pressure return promptly to the normal upon the cessation 
of work. With a diseased cardiovascular system this is not so 
promptly accomplished. The heart which has been weakened by 
infectious processes shows a wide range and a prolonged duration 
of pulse and blood-pressure variations. The amount of psychic 

1 Barach, Jos. H., and W. L. Marks, Effect of Change of Posture, without Active 
Muscular Exertion, on the Arterial and Venous Pressures, Archiv. Int. Med., May 
15, 1913, ii, No. 5. 



150 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

effort required is of the greatest importance. Work which is per- 
formed passively, automatically, without any particular psychic 
concentration, is not accompanied by a rise in tension. The primary 
fall of pressure which occurs under training is, largely the result 
of eliminating the volitional psychic factor. An increase of pressure 
under muscular work depends more on the cerebral stimuli required 
than on the amount of work done. In the hypnotized subject, 
imaginary work produced an elevation of pressure to 200 mm. 
Hg. (Klemperer). These causes explain many of the failures of 
testing functional capacity by measured amounts of work. Although 
we can measure the work performed in kilogrammeters we have no 
means of estimating the amount of neryous force and psychic 
energy which may be expended upon the same task by different 
classes of trained and untrained, nervous and phlegmatic, energetic 
and lazy individuals (see p. 367). 

The increase of pressure which is associated with muscular effort 
affects chiefly the systolic pressure; the diastolic element tends to 
lag behind, thus increasing the amplitude of the pulse. On assum- 
ing the erect posture the minute volume decreases slightly, the 
systolic output greatly (20 per cent.). In the recumbent pos- 
ture the minute volume in women increases 17.2 per cent., 
and the systolic output 31 per cent. In men this change was not 
observed owing probably to a more efficient vasomotor system. 1 
Lowsley 2 found that physical activity caused a rapid rise in blood- 
pressure which precedes the increase of the pulse rate. During con- 
tinued exercise these curves show but little change. After cessation 
from work the fall in the systolic pressure again precedes the 
decrease in the pulse rate. A secondary rise of the pulse rate occurs 
which is a " reflex effort due to low blood-pressure of the subnormal 
stage." 

Muscular effort sufficient to increase the pulse rate provokes 
a rise of the systolic, diastolic and the venous pressures. Inasmuch 
as the systolic pressure rises more than the diastolic, the pulse 
pressure is increased. 

Following the primary maximal rise of systolic pressure a gradual 
decline occurs, but while exercise is being continued the pressure 
never reaches the normal level. The diastolic pressure generally 

1 Lindhard, J., Effect of Posture on the Output of the Heart, Skand. Arch. f. 
Physiol., 1913, xxx, 395. 

2 The Effects of Various Forms of Exercise on Systolic. Diastolic, and Pulse Press- 
ures and the Pulse Rate, Amer. .lour, Physiol., 1911, xxvii, 446. 






CRAVPNER'S TEST 151 

follows the systolic curve but its maximum is reached later and 
upon cessation from work it invariably falls below its normal level. 
According to Lowsley the longer the subnormal diastolic phase, 
the greater the circulatory fatigue. The venous pressure shows 
often a sudden drop to normal after cessation from exercise. Exer- 
cise associated with strain requiring a closed glottis and a rigid 
chest, disproportionately increases blood-pressure in relation to 
the pulse rate and very markedly increases venous pressure. 

Graupner's Test. — Graupner 1 endeavored to test cardiac func- 
tionation by noting the effects of measured work upon the pulse, 
the blood-pressure and the size of the heart, the blood-pressure 
being measured with a Gartner tonometer and taken when the 
pulse had reached the same rate, after the exercise, which it had 
before this was commenced. His investigations led him to the 
following conclusions: (1) Blood-pressure remains constant — 
cardiac sufficiency. (2) Blood-pressure falls — cardiac insufficiency. 
(3) Blood-pressure rises, but 'returns to normal — compensatory 
capacity. (4) Blood-pressure rises, falls rapidly, without a ten- 
dency to rise again — fatigue. 

He insists that the work must be done by the same muscle groups, 
preferably the thighs; and must not be carried to the degree of 
exhaustion, as this necessitates the introduction of other cardio- 
accelerator impulses, such as psychical effort, excess of metabolic 
waste products in the blood, etc. There must be no muscular 
strain, thoracic encumberment or unnecessary mental excitement. 
He prefers the Zuntz ergometer, 2 built on the principle of the 
bicycle, to the Gartner ergostats, 3 on account of its greater accuracy. 

The work consisted in having the patient turn a wheel supplied 
with a brake with which work could be measured. The tests were 
made at the same hour on successive days, the relation to meal- 
time being constant. He fully recognized the fact that apparent 
incapacity of the heart may be due to lack of training, owing to 
the fact that definite kinds of work may be performed by the skeletal 
muscles with much less cerebral and muscular fatigue after the 
individual has become habituated to the exercise, and the centres 
in the medulla have become used to increased quantities of carbon 
dioxide in the blood. Furthermore, even the diseased heart, unless 
compensation is extremely bad, may increase in power upon exercise. 

1 Graupner, Die Mechanische Priifung und Beurtheilung dor Herzleistung, Berlin. 
Klin., 1902, xv, No. 174. 

2 Zuntz, Centralbl. f. Physiol., 1S98, p. 502. 

3 Gartner, Allg. Wien. med. Zeit., 18S7, Nos. 49 and 50. 



152 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

Graupner believes, as the result of his investigations, that both in 
functional and organic incapacity of the heart, accelerated pulse 
rate and dyspnea are caused by the performance of work equiva- 
lent to from 45 to 300 mkg. per minute. In myocarditis less than 
the last-named figure is invariably sufficient to produce these symp- 
toms, whereas, in merely functional incapacity more is often 
required. The same method of differentiation holds good between 
angina pectoris of sclerotic and of nervous origin. 



EECINrv 


INC. OF WORK 
























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D 


OF 


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J 


HG.14 












































































































































b 








u 






d 






































13 
















































j 








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11 

10 














































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i 












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/ 




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S 


















































































































































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Fig. 68. — 1. When functional capacity is good the blood-pressure undergoes 
practically no change during exercise, or if severe effort is required rises slightly. 
Fluctuation begins thirty seconds after cessation from work. 

2. Immediately upon cessation from more strenuous work, blood-pressure is 
slightly elevated, but soon falls to the normal. The rapidity of this fall may be 
increased by training. If insufficiency exists, the elevation is greater, persists longer, 
and the normal is more slowly reached (hi, a-i, 03). 

3. More severe effort may produce a fall of pressure while work is going on, in 
which case it promptly rises to the normal after cessation from work (6). 

4. Still more work may cause a lower fall, which is later followed by a rise above 
the normal (c, d). 

5. The absence of this secondary rise even after repeated or more prolonged work 
bespeaks myocardial fatigue. In such cases we will usually find clinical signs of 
insufficiency (e). 

6. The onset of dyspnea may reflexly produce increased blood-pressure, but in 
such an event we soon find a fall far below the normal. 

7. Conclusions must not be drawn from one set of observations alone, but if 
evidences of insufficiency are persistently encountered, we may feel reasonably 
sure that we are dealing with heart weakness; for if these findings were due to 
vasomotor influences they would disappear under "training." 



The glaring faults of Graupner 's method are (1) that we cannot 
determine the amount or eliminate the effects of psychical and 
visceral influences upon the pulse and blood-pressure, although 
the author claims that by this joint observation the one controls 
the other; (2) it is necessary to make each test twice to see if the 
heart will respond the second time as it did the first, and, further- 
more, we have no means of estimating the effects of the peripheral 



KATZENSTEIN'S TEST 153 

vessels. Finally, that all tests which are based upon an estimation 
of the pulse rate or blood-pressure do not take into account the 
normal rhythmic periodic fluctuation which these as well as other 
factors of the economy are subject to. 

Graupner and others who have investigated the question have 
found that a fall in tension after exercise indicates insufficiency, 
or at least fatigue. Butermann also found that well-compensated 
valvular lesions and neurotic hearts responded to exercise by a 
rise of blood-pressure averaging 13 mm., whereas myocardial cases 
showed a lessening of tension varying from 3 to 13 mm. 

Since the appearance of his original paper Graupner 1 has been 
continuing his researches, and in a more recent article he reiterates 
his convictions, laying special stress upon the value of blood- 
pressure measurements. Regular changes in this indicate that the 
myocardium is able to adjust itself to the existing conditions. Ac- 
cording to his observations normal hearts can perform arm-muscle 
work on the ergometer equivalent to from 3000 to 20,000 mkg. 
per hour. If the figures fall below 1000 mkg. absolute myocardial 
weakness exists, while a capacity of less than from 200 to 500 mkg. 
offers a bad prognosis as to life. When a certain group of muscles 
is exercised the blood is drawn toward them at the expense of the 
other vascular areas. To restore the balance later, the blood rushes 
away and pressure falls, to be followed by a return wave which 
in its turn abates. When measurements are made every half- 
minute after exercise it has been found that the amount of variability 
in the blood-pressure corresponds directly with the insufficiency 
of the myocardium. In other words, the greater the heart weakness 
the wider the pressure fluctuations, and the longer is the time 
required for the restoration of balance (Fig. 67). 

Some other observers have found that pressure falls in the case 
of well-trained athletes which, according to Graupner's contention, 
would indicate cardiac insufficiency, whereas a rise of pressure 
occurs in some cases of patients with diseased hearts as a result of 
high-pressure stasis. As Hoffmann has shown, the test often fails 
us when most needed — in the differentiation of neuroses from 
organic lesions. 

Katzenstein's Test. — This test for determining the degree of 
functional capacity of the heart is based upon the manner in which 
this organ responds to compression of both iliac arteries. 2 

1 Deut. med. Woch., 1906, xxxii, 1029. 

2 Katzenstein, Berlin, klin. Woch., 1907, xliv, No. 16. 



154 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

Experimentally in animals, if some of the large vessels are 
obliterated, blood-pressure rises while the pulse rate remains sta- 
tionary. In human beings it was" found that if the heart was 
functionally potent, bilateral obliteration of the iliac arteries, main- 
tained for from two to five minutes, caused a rise in blood-pressure 
of from 5 to 15 mm. of mercury; the pulse rate remained stationary 
or even diminished. In the case of an hypertrophied heart, with 
good compensation, the blood-pressure rises perhaps to 40 mm., 



120 


a 








110 / 


^\ 


100 7 




e 


/ / 

/ / 

90 / / 






on JLLS 




' \ 







a 








b 



Fig. 69. — The absolute sphygmogram. If the cuff pressure be raised to 100 mm. 
Hg. only that part of the pulse wave which is in excess of this pressure will be traced 
(see page 146). 



the rate being still unaffected. If there is slight insufficiency, the 
pressure does not rise, whereas the pulse does become accelerated. 
In severe insufficiency the pressure falls and the pulse becomes 
more rapid. These tests are made with the subject in the recumbent 
posture. The sources of error in this method are manifestly mental 
excitement, and the possibility of producing pain during the com- 
pression of the arteries, either of which might seriously militate 
against the accuracy of the results; but with due care both of these 
factors may be eliminated. 



THE VENOUS PRESSURE TEST 155 

\\ ith a view toward investigating Katzenstein's test, the author 1 
studied a number of cases both among healthy individuals and 
among those in whom cardiac weakness or disease was assured. 
As the result of these investigations it was found that, generally 
speaking, the cases responded to the test as has been contended 
by the deviser of it. There were, however, notable exceptions in a 
number of instances. Although the majority of cases with manifest 
cardiac weakness responded positively to the test, yet — and here 
lies the main ground for objection — many of them did so in such 
equivocal terms, that is, by such small changes in the pulse rate 
or blood-pressure, that the final decision was left largely to the 
personal equation of the observer. Morelli 2 suggests that compres- 
sion be exercised by means of inflated rubber stockings. In a 
recent communication based upon three thousand cases, during 
the last ten years, Katzenstein 3 reiterates his belief in the efficacy 
of his test. He has found it of especial value in discovering cardiac 
weakness in operative cases in which chloroform was subsequently 
used as an anesthetic. 

This test has been investigated by numerous writers. It may 
at times have some corroborative value, but much dependence 
should not be placed upon it. A test based on the same general 
principle has been suggested by Mosler, 4 who estimates the blood- 
pressure after a deep forced inspiration at the conclusion of which 
the breath is held. 

Janowski, 5 who tested his patients by (1) walking one thousand 
steps in twelve minutes; (2) the rapid climbing of three flights of 
stairs; (3) knee flexion while standing, twelve times at a given tempo ; 
meanwhile observing the blood-pressure and pulse rate at intervals 
up to ten minutes after the completion of the task, failed to find 
differences which corresponded to the individuals studied. Neither 
pulse rate, blood-pressure, pulse pressure, nor blood-pressure 
quotient yielded the differences which he was led to expect. 

The Venous Pressure Test (Schott's 6 Test). — It appears that in 
health if the patient raises his arm to an angle of 60 degrees while 

1 Norris, G. W., The Functional Capacity of the Heart, Internat. Clinics, vol. i, 
Series 17. 

2 Delia Capacita Funzionale del cuore e dei Vasi Sanguini, Boll. Soc. Med. Chir. 
di Pavia, March 12, 1910. 

3 Deut. med. Wchnschr., 1915, vol. xli, No. 16. 

4 Der Atemstillstand in tiefer Inspirationsstellung: Ein Versuch z. Beurteilung 
der Kreislauffunktion, Zeit. f. klin. Med., 1913, lxxviii, 133. 

6 Die Funktionelle Herzdiagnostik, Berlin, 1910. 

6 Die Erhohung des Druckes im venosen System bei Anstrengung als Mass fiir 
die Funktionstiichtigkeit des menschlichen Herzens, Deutsch. Arch. f. klin. Med., 
1912, cviii, 537-553. 



156 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

lying quietly without any other muscular effort, the venous pressure 
shows on an average an increased pressure of 0.5 cm. H2O (sometimes 
no increase, nor even a fall). In well-compensated heart lesions the 
increased pressure averages 2.3 cm.; in broken compensation, 4 
to 7 cm.; in conditions of anasarca, etc., 7.3 cm. He therefore 
considers figures above 3 cm. as pathological. Passive elevation 
of the limb produces no increase of venous pressure. 





Fig. 70. — Absolute sphygmograms and pulse tracings from a ease of marked 
hypertension and from a ease of marked hypotension. Showing that the pulse 
tracing gives a very inaccurate representation of the actual height of the arterial 
pressure. (After Gallavardin.) 

The Absolute Sphygmogram. — The information obtainable from 
the pulse tracing alone, so far as blood-pressure is concerned, is 
slight because: (1) we do not know the actual value of the abscissa 
and (2) because the actual length of the waves depends largely on 
the adjustment of the sphygmograph (amount of pressure exerted 
on the underlying artery). 



THE ABSOLUTE SPHYGMOGRAM 



157 



In 1904 Sahli suggested a method for plotting the sphygmogram 
in absolute pressure values. His method depends upon the fact 
that if sphygmograms are taken from the radial artery while a 
blood-pressure cuff is applied to the brachial artery above with 
increasing pressures, the sphygmogram will be traced of only that 
portion of the pulse curve corresponding to intra-arterial pressures 
higher than the pressure in the cuff. Thus, if Fig. 69 represents 
the actual pressure curve of the pulse in the artery, if the pressure 

















































21(1 


MX 








































2011 














































mo 














































if ii 














































170 

160 

150 






















































































































140 1 




































130 
120 






































































110 

100 


lMlMiii 


I 


: 


UN 








no 
















































00 




































so 
































70 


























60 
















ill 




50 




















10 






















80 






















20 






















10 










































































i 
































1 








Fig. 71. — Absolute sphygmogram and pulse tracing from a case of hypertension 
and from a case of hypotension. (After Gallavardin.) 



in the cuff be raised to 100 only that portion of the pulse curve 
drawn heavy and corresponding to pressures above 100 will be 
traced. It is therefore possible, by altering the pressures in the cuff 
and noting the amount of the sphygmogram traced at each pressure, 
to determine the absolute pressure of any point on the pulse 
curve. 

The time relations of these points may be determined from the 
sphygmogram. The curve may then be plotted on cross-section 



158 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

paper, allowing the vertical lines to represent time units and the 
horizontal lines units of blood-pressure. It is only from such a 
curve that the true mean pressure can be determined. Thus, if 
the length of a sufficient number of equally spaced vertical lines 
from the base line a-b to the pressure curve c, d, e, f, g, be measured 
and their average taken, such average will be the true mean pressure. 
For clinical purposes Sahli constructs a simplified form by plotting 
only the systolic pressure or crest of the pulse curve (d), and the 





Fig. 72. — Showing absolute sphygmogram and pulse tracing from a subject with 
normal blood-pressure, and that of a case of nephritic hypertension. (After Galla- 
vardin.) 



diastolic pressure or lowest point of the pulse curve (c and g), thus 
obtaining the dotted figure a, c, d, g, b. From such a diagram one 
can judge accurately as to the quickness or slowness of the pulse 
(pulsus celer, or pulsus tardus). 

The Blood-pressure Quotient. — Let us assume that the data 
obtained regarding systolic and diastolic pressures are correct. 
What conclusions are we warranted in drawing regarding the 
amount of work performed by the heart and the amount of its 



THE BLOOD-PRESSURE QUOTIENT 159 

systolic output? The question has recently been ably summarized 
by O. Muller, 1 from whose article I have freely drawn. 

Strassburger has shown that the pulse pressure divided by the 
systolic pressure is of value in estimating the part played by vascular 
resistance and cardiac work respectively, in changing circulatory 
conditions. 

The rationale of the method is as follows: With increased cardiac 
work, the pulse pressure as well as the systolic pressure increases. 
If, on the other hand, peripheral tonus alone increases, the systolic 
pressure rises, while the pulse pressure falls. Vasodilatation pro- 
duces a fall of systolic pressure and an increase of pulse pressure. 
Therefore if the systolic pressure and the pulse pressure move in 
the same direction and proportionately, the cause lies in the heart; 
if in the reverse direction, or not proportionately, the cause lies at 
least partly in changes in vascular tonus. The cardiac element 
is also indicated by the number of systoles. 

Pulse pressure 

B. P. Q. = o . ,. = (normally about 0.3). 

Systolic pressure 

1. A changed systolic pressure while the quotient remains the 
same points to a change in the work of the heart. If both systolic 
and pulse pressure rise, an increased; and if both fall, a diminished 
cardiac activity may be assumed. 

2. When systolic pressure and blood-pressure quotient move 
in approximately equal but opposite directions, indications point 
to an alteration of vascular tone. Thus an increase in systolic 
pressure with a fall of quotient = increased tonus and vice versa. 

3. When systolic pressure and quotient move unequally in the 
same or in opposite directions, both the heart and the vascular sys- 
tem contribute to the effect. With the limitations imposed by the 
response of the pulse pressure to factors other than the systolic 
output (already considered on page 50), and if our estimation of the 
systolic and diastolic pressures be accurate, these assumptions 
are warranted. The variations of aortic elasticity for different 
degrees of pressure are clinically a negligible quantity. But a far 
more serious source of error lies in the fact that the smaller arteries 
and arterioles possess a distinct tonus, the amount of which we are 
as yet unable to measure. If the arterial system merely consisted 
of rubber tubing our figures would certainly be at least approxi- 
mately correct, and our deductions correspondingly accurate; 

1 Die unblutige Blutdruckmessung u. ihre Bedeutung f. d. prakt. Med., Med. 
Klinik., January 12, 1908, p. 47, et seq. 



1(50 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

in illustration of this it has been demonstrated that in cases of 
arteriosclerosis the pulse pressure is often twice as large as in a 
normal individual, but we have no right to conclude from this 
that in such a case the systolic output is correspondingly great. 
It is far more likely in such an instance that the difference is due 
to the rigidity of the arterial wall. The pulsatory reaction of a 
contracted artery is entirely different from that of a relaxed artery 
of the same caliber. Again, as F. Klemperer has shown, if we dip 
one arm into hot and the other into cold water, the pulse pressure 
will be found to decrease in the former and to increase in the latter; 
and yet we know that cold produces vascular contraction. Which of 
the two sides shall we choose as the index of systolic cardiac output? 

It may be argued in reply that such extremes as the hot and 
cold water experiment do not occur under normal conditions, but 
notwithstanding we must bear in mind the fact that plethysmo- 
graphic studies have indubitably demonstrated the fact that fre- 
quent and often extensive vasomotor changes are going on more 
or less constantly in the normal human economy, especially as 
the result of pain, psychic influence or temperature change, all of 
which are apt to enter into an ordinary blood-pressure estimation. 

Fuerst and Soetbeer 1 suggest that the Strassburger formula be 
modified to read: 

Pulse pressure 

Diastolic pressure + 3 pulse pressure 



believing that the pressure variations in the aorta are thus more 
nearly portrayed. 

Applying a table originally devised by Beanus, Erlanger and 
Hooker indicate the deductions to be drawn as to cardiac activity 
and vascular resistance from blood-pressure, pulse pressure, and car- 
diac rate as follows. Since the mean pressure follows the diastolic 
more closely than the systolic they recommend the former as the 
indicator of blood-pressure in the table. 



Deternii 

Diastolic 
pressure. 


nable factors. 

Pulse pressure 

X pulse rate 

(velocity of flow). 


Constant 




Increased 

Diminished 

Unchanged 


Increased . 




Increased 
Diminished 


Diminished 




Unchanged 

Increased 

Diminished 



Causative 


factors. 


Energy from 


Peripheral 


heart. 


resistance. 


Increased 


Diminished 


Diminished 


Increased 


Increased 


Increased 


Increased 


Unchanged 


Unchanged 


Increased 


Diminished 


Diminished 


Unchanged 


Diminished 


Diminished 


Unchanged 



1 Untersuchungen u. d. Beziehungen aw. Fuellung u. Druck. in d. Aorta, Deut. 
Arch. f. klin. Med., 1907, vol. xc. 



THE AMPLITUDE-FREQUENCY PRODUCT 1(31 

The table, however, is too diagrammatic to be of value except 
as an illustration of the general principles involved. For example, 
cases of nephritic hypertension with increased peripheral resistance 
and a compensatory increase of cardiac activity show commonly an 
increase both of diastolic pressure and of pulse pressure X pulse rate. 
The table would interpret such an effect upon the blood-pressure, 
pulse pressure and pulse rate as indicating increased cardiac activ- 
ity, but unchanged peripheral resistance — an entirely erroneous 
interpretation. This limitation in the table is of course due to the 
fact that it deals with changes in the various factors only as to the 
direction of the change (whether increased or diminished), and not 
as to the degree of the change. 

Velden found that if the two foregoing formulas — Strassburger's 
and that of Erlanger and Hooker — were applied to the same case 
they often led to diametrically opposite conclusions. 

The Energy Index. — Barach 1 found that what he terms the energy 
index (S. D. R. Index) is useful as a clinical estimation of the 
amount of cardiovascular energy expended, e. g. : 

Biood-pressure. Pulse rate. Index. 
Systolic pressure . 120 mm. Hg. X 72 = 8.640 
Diastolic pressure . 70 " " X 72 = 5 . 040 

Energy index \ .„- „ „ . . - n no „ M , TT 

/ i u \ t ■ 190 X 72 = 13.680 mm. Hg. per nun. 

(sum of above) J b * 

The highest energy index in normal cases is about 20,000 mm. 
Hg. per minute. In pathologic cases figures as high as 50,000 were 
encountered. A considerable number of the cases with high indices 
died of apoplexy. 

The Amplitude-frequency Product. — Yon Recklinghausen 2 ap- 
proaches the question from a different direction, yet reaches 
conclusions somewhat similar to those of Strassburger. For him 
the vascular system consists of two reservoirs; the smaller pulsating 
(arterial) and the larger continuously flowing (venous). The 
circulation between the two by means of the capillaries is not 
directly affected by cardiac activity. He assumes that to a certain 
extent at least the diastolic blood-flow occurs as in a series of stand- 
pipes, according to Poiseuille's law. He believes that to a certain 
degree the diastolic limb of the pulse wave can be shown to be 

1 The Energy Index, Jour. Amer. Med. Assn., 1914, lxii, 525. 

- Was wir durch d. Pulsdruckkurve u. d. Pulsdruckamplitude liber d. grossen 
Kreislauf erfahren, Arch. f. exp. Path. u. Phar., 1906, hi. 
11 



162 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

identical with an ordinary outflow curve.' He assumes that the 
arteries themselves are not actively concerned in the propulsion 
of the blood-stream. 1 

Now, if we register the pulse wave from a brachial cuff with a 
tambour manometer at a certain pressure, we shall find the curve 
indicating a certain relationship between the amount of blood 
propelled in a given time and the elasticity of the artery. Since 
it is not always feasible to take a tracing and lay off an absolute 
sphygmogram, he suggests as a practical method the amplitude 
(pulse pressure) multiplied by frequency (pulse rate) = seconds 
volume -f- arterial dilatability; in other words amplitude multiplied 
by rate is proportionate to systolic output divided by distensibility. 
Thus, if we can be sure that distensibility remains unchanged, then 
amplitude is a relative measure of systolic output. But how are 
we to gauge this factor of distensibility? Von Recklinghausen 
suggests that the following axioms may throw some light on the 
question: 

1. With a constant pressure and with increasing tonus the dis- 
tensibility of the artery diminishes. With a decrease of tonus, it 
increases. 

2. Increased arterial tension generally goes hand-in-hand with 
increased vascular tonus. We thus in all probability have a doubly 
decreased distensibility. 

3. In sclerotic arteries the relative distensibility of bloodvessels 
is diminished. 

We must not use the rules of Strassburger's blood quotient too 
absolutely. It is evident that we can draw no mathematically rigid 
conclusions from changes of pulse pressure even in the same indi- 
vidual, and much less can we hope to use the data thus obtained 
in comparison with other individuals. We cannot by any rule con- 
vert millimeters of pulse pressure into cubic centimeters of systolic 
output. It has been shown that in the case of the diseased heart 
which is manifesting fatigue, the amplitude-frequency product in- 
creases less rapidly than in health; it may indeed be entirely 
lacking. Tiedemann, who compared the amplitude and the ampli- 
tude-frequency product in healthy and diseased hearts after the 
lifting of weights, found that in the former case both of these factors 
increased, while in the latter they did so to a lessened extent or not 

1 This belief has been much questioned of late, based on the observation of Gruetz- 
■ ner that with an equal amount of pressure applied to an artery, more blood can be 
forced out in the direction of normal flow than in the opposite direction. 



METHODS OF EST I MAT ISC THE RATE OF BLOOD-FLOW 163 

at all. These results were indubitable, but what construction should 
be put upon them was less clear. Without a knowledge of the state 
of the vascular tonus no actual figures could be obtained. 

METHODS OF ESTIMATING THE RATE OF BLOOD-FLOW. 1 

While a knowledge of the state of the blood-pressure is often of 
great value, it gives us no clew as to the rapidity of the circulation 
— the mass movement of the blood. A high vascular tension may 
be associated with a small blood-flow and vice versa; for the rapidity 
of the circulation depends not only upon arterial pressure but 
also upon the caliber of the vessels between artery and vein, and 
under some circumstances upon venous pressure. It has been 
shown that the circulation rate increases in proportion to the oxygen 
consumption in a manner corresponding to the increase in total 
ventilation; and it has been suggested that the chief controlling 
factor of the circulation rate is the hydrogen ion concentration of 
the arterial blood. 2 

G. N. Stewart 3 has devised a method of determining the rate 
of flow which depends on the fact that "the amount of heat pro- 
duced by a part like the hand during rest is negligible in comparison 
with the heat conveyed to it by the arterial blood. If, then, we 
determine the amount of heat given off by the hand to a calorimeter 
in a given time, and know the temperature of the incoming (arterial) 
and of the outgoing (venous) blood, we can calculate how much 
blood must have passed through the hand in order that it might 
give off this amount of heat. The quantity of heat given off is 
estimated by putting the hand into a calorimeter." 

" It consists of an inner copper vessel containing a known amount 
of water (in the experiments usually about three liters), into which 
the hand is inserted through an orifice of appropriate size and shape 
in the lid, heat-tight closure being made by the collar of thick 
felt on the top of the calorimeter. The inner vessel is packed 
in broken cork in a larger outer vessel and the lid is covered with 
sheet cork to reduce as far as possible the loss of heat, and to 
protect the calorimeter against irregular cooling when exposed to 
draughts. The actual loss is estimated by separate control experi- 

1 See page 35. 

2 Boothby, Walter M., A Determination of the Circulation Rate in Man at Rest 
and at Work, Am. Jour. Physiol., 1915, xxxvii, 383. 

3 Measurement of the Rate of Flow of the Blood in Man, Cleveland Med. Jour., 
April, 1911, x, 385; Studies on the Circulation in Man, Heart, October, 1911, iii, 33. 



164 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

ments, and added to the amount of heat given off by the hand as 
indicated by the rise of temperature in the water. The hand is 
prepared for insertion into the calorimeter by a preliminary immer- 
sion for not less than ten minutes in a large bath containing water 
at approximately the same temperature as that in the calorimeter. 
The temperature of the water in the calorimeter is read on a ther- 
mometer permitting hundredths of degrees to be accurately 
estimated. The calorimeter is mounted on a stand which can 
be raised or lowered by a screw to permit its use either for a 
patient sitting in bed or for an ambulatory patient who is able 
to sit in a high chair. As a general rule the flow in the two hands 
is simultaneously measured. The quantity of blood in grams 
flowing through the hand in the time of the experiment is given 
by the formula: 

H 1 

Q = t^t* x 7" 

"Here Q is the quantity of blood, H the heat given off by the 
hand, T the temperature of the arterial blood, T 1 the tempera- 
ture of the venous blood, and s the specific heat of blood. In 
estimating H the water equivalent of the hand itself (obtained 
by multiplying its volume by 0.8) and the water equivalent of 
the calorimeter (80 grams) must be added to the quantity of 
heat corresponding to the actually observed rise of temperature. 
The specific heat of blood is taken at 0.9. Knowing the volume 
of the hand, we can express the flow in grams per minute per 
100 c.c. of hand substance. The volume of the hand is easily 
estimated by the amount of water which it displaces when 
immersed in a glass douche-can to the level to which it was 
inserted in the calorimeter. The douche-can is connected by 
the tubulure to a burette, on the scale of which the vertical dis- 
placement of the water is read off. The amount of water which 
must be added to that in the can in order to give the same level 
in the burette is clearly the volume of the hand. The distance 
to which the hand is to be inserted into the calorimeter is fixed by 
making a horizontal mark with a pencil at the level of the lower 
border of the styloid process of the ulna. A parallel mark is drawn 
above this at a distance equal to the combined thickness of the 
felt collar and the lid of the calorimeter, and this second mark 
is just kept in view above the collar during the experiment. The 
lower mark must then define the limit up to which the hand is 



METHODS OF ESTIMATING THE RATE OF BLOOD-FLOW 165 

enclosed in the calorimeter. The collar is supported by a flange 
around the orifice. The temperature of the arterial blood at the 
wrist is taken as 0.5° below the rectal temperature, since this was 
the difference actually found in a normal person. It can be measured 
by determining that temperature of the calorimeter at which the 
hand neither gains nor loses heat. Where the rectal temperature 
cannot be conveniently obtained the mouth temperature is taken 
as that of the arterial blood at the wrist. The temperature of the 
venous blood is taken as the average temperature of the calori- 
meter during the experiment, since direct estimations of the tem- 
perature of blood collected by puncture of hand veins, during 
immersion of the hand in baths at known temperatures, showed 
that the excess of the temperature of the venous blood over that of 
the bath was so small as to be negligible for such bath tempera- 
tures as are used in the experiments." 

The normal average flow as determined by Stewart ranged 
between 3.5 and 14 grams of blood per 100 c.c. of hand per minute 
at ordinary room temperature, and with an immersion of ten or 
fifteen minutes. Individual variations on different days were 
more or less constant. Elevation of the room temperature increased 
the flow. Muscular activity of one hand produced an increase of 
flow in that member over its fellow in proportion of nearly three 
to one. Individuals with habitually cold hands exhibited a lower 
rate of flow than normal people. A diminished blood-flow also 
results from venous stasis produced by moderate constriction of 
the wrist. The local application of heat increases the rate of 
flow. 

Even a moderate amount of forced breathing decreases blood-flow, 
in explanation of which Stewart suggests "acapnia caused by the 
washing out of the carbon dioxid as a possible influence. Mechan- 
ical changes in the thorax, and particularly those affecting the 
filling and discharge of the heart, must also be taken into account. 
One moral to be drawn is that while the respiratory pump has a 
part of some consequence in the normal movement of the blood, 
and may even become the preponderant factor when the heart 
and the vasomotor mechanisms are crippled, the idea of the "deep- 
breathing" fanatics that voluntary interference with the delicately 
regulated respiratory mechanics must be good receives no support, 
at least so far as the circulation in the periphery is concerned." 

Further findings regarding the rate of flow showed a diminished 
rate in cases of arteriosclerosis of long standing; of brachial neuritis 



166 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

with muscular atrophy; and of hemiplegia (associated with complete 
abolition of vasomotor reflexes on the affected side). 

An increased flow was found in early peripheral neuritis on the 
affected side, probably owing to a paresis of the vasoconstrictor 




Fig. 73. — The plethysmograph: A, cuff; B, recording tambour; C, chronograph; 
D, drum. (After Hoffmann.) 



fibers; in a case of occupation neuralgia; in case of an infected 
finger (with partial obliteration of vasomotor reflexes); in exoph- 
thalmic goitre. 

The Plethysmograph. — This instrument gives us information 
regarding the volume pulse. The volume of all organs varies with 



METHODS OF ESTIMATING THE RATE OF BLOOD-FLOW 167 

the different phases of the cardiac cycle with those of the respira- 
tion and with vascular tonus, as well as with certain psychic 
influences, etc. 

The Method. — The extremity to be investigated, generally the 
forearm, is introduced into a glass chamber which is filled with 
water and made water-tight by means of a rubber cuff. The water 
contained in the cylinder communicates by means of rubber tubing 
with a recording piston, the upward or downward displacement 
of which imparts its fluctuations to a tambour which records 
its movement on a kymograph. By this means the variations in 
volume may be studied. 

The technique is somewhat complicated, and hence the plethys- 
mograph is hardly likely ever to become a popular instrument 
for clinical work, but for purposes of scientific investigation, 
therapeutic effects, etc., it possesses a distinct field of usefulness 
(Fig. 73). 

The actual amount of blood in the arm can be estimated as suggested 
by O. Miiller, 1 by rendering the limb bloodless by immersion in 
mercury, and then applying an Esmarch bandage to the upper 
arm, the constriction of which is not released until the plethys- 
mography adjustment has been made. The method is not 
infallible, however, as the primary anemia tends to the production 
of a secondary hyperemia. Some interesting results were obtained 
with the plethysmograph by Weber, who was able to show the 
effect of psychic stimuli on blood distribution. For instance a 
concentration of attention upon the arm — the subject being told to 
imagine he was performing muscular actions with it — is attended 
by an increased flow to the part. 

Miiller has constructed the following table showing the effects 
of different stimuli on blood distribution: 













Periphery 


Abdominal 


Extremities 


Brain. 


of head. 


organs. 


etc. 


Cold + 


— 


+ 


— 


Warmth 








— 


+ 


— 


+ 


Chloroform 








+ 


— 


+ 


— 


Adrenalin . 








+ 


— 




— 


Desire . 








+ 


+ 


— 


+ 


Disgust 








— 


— 


+ 


— 


Fright . . 








+ 


— 


+ 


— 


Mental effort 








+ 


— 


+ 


— 


Sleep 








+ 


+ 


— 


+ 


Imaginary exer 
oer. u. kritisehf 


cise 
B< 


s 

">i tr. 


tao. 


+ 
zur mode 


•nen TCreislfinf 


Dinjmostitc 1 


+ 
i_ ihr wpifrpr 



Ausbau durch Einfiihrung des absoluten Plethysphygmogrammes, Verhandl. d. 
Kong. f. inn. Med. Wiesb., 1907, xxiv, 384. 



168 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

A small finger plethysmograph has been devised by Fleischer. 1 
It must be borne in mind that deductions drawn from plethys- 
mographic readings can be applied only to the limb in ques- 
tion, not the system as a whole. Particularly useful data may 
be obtained if such observations are made simultaneously with 
blood-pressure observations (Fig. 74). 

The plethysmograph gives us data regarding the peripheral 
circulation but tells us nothing as to the underlying causes which 
produce them, as to whether variations are due to an abnormal 
elasticity, or a small arterial bed, and as to whether these changes 
are normal for the individual or pathologic manifestations. How 
great a part is taken by vasomotor tone, and whether the stimuli 
causing these changes arise in the spinal cord or in the peripheral 




Fig. 74. — The finger plethysmograph. (Fleischer.) 



ganglia, or whether the fault lies in the capillaries or veins, upon 
these questions we vainly seek for information. 

A. Muller 2 has suggested that systolic output might be gouged 
by the determination of the venous pressure. 

« Berlin, klin. Woch., 1908. 

2 Ueber Sehlagvolumen u. Herzarbeit des Menschen, Deut. Arch. f. klin. Med., 
1909, xcvi, 127. 



METHODS OF ESTIMATING THE RATE OF BLOOD-FLOW 1G9 

The Method. — The circulation in the arm is arrested by the 
sudden inflation of the brachial cuff from a large bottle containing 
air under pressure. The venous pressure is now measured by the 
Basch-Recklinghausen method, which gives us the resistance (W) 
which the succeeding arterial pressure must overcome. The arm 
is next placed in a plethysmograph above which another cuff is 
applied and inflated to about 50 mm. Hg., a pressure well below 
the minimum pressure and which therefore does not interfere with 




Fig. 75.- 



-Plethysmographic curve used to determine Vi (the arterial flow into the 
arm, against the resistance W). 



arterial inflow, although it does with venous outflow. The pressure 
in the upper cuff is now suddenly dropped to 0, the arterial blood 
flows into the arm but cannot flow out of its vein until the venous 
pressure rises above that in the cuff (50 mm.). Until this occurs 
the arm is in a hydrostatic condition and the resultant sphygmo- 
graphic curve will be a curve of arterial outflow (F) (Fig. 75). 

Under these conditions the pressure in the occluded region will 
be a measure of the resistance (IF) against which the outflowing 
blood-stream operates when the obstruction is removed. The 



170 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

second cuff which measures the venous pressure does not interfere 
with the inflow but prevents for a time the onward flow of venous 
blood. The height of the first volume pulse indicates the value 
of V. If bodily weight and mean pressure are known, we can 
calculate V the systolic output, and V D, the cardiac work. 

Using this method Muller found that the systolic output averaged 
85 c.c. for men and 25 c.c. for women. An increase was found in 
nephritis, cardiovascular disease, exophthalmic goitre, and Addison's 
disease. 

This method has been criticised as theoretically faulty by Christen 
and the practical results have varied considerably from those of 
Plesch. 1 

A somewhat similar method of procedure, based on the method 
of Brodie, 2 has been proposed by Hewlett and Van Zwaluwenburg, 3 
to determine the rate of blood-flow (Fig. 76). 

The arterial blood enters the organ with undiminished speed 
at first, but soon the flow is retarded by the rise of pressure in the 
veins and capillaries. The organ therefore swells rapidly at first 
and progressively more slowly. The earliest portion of this curve 
represents the rate at which the blood enters under normal con- 
ditions. Brodie has shown that this method gives as reliable 
results as the Stromuhr. 

The following method of testing the circulation time has been 
suggested by Bornstein. 4 The patient is made to breathe C0 2 and 
the time is noted at which the respirations become more forcible. 
This indicates the time taken by the blood to pass through the 
lung and left heart and to reach the respirator}- centre; it is assumed 
to be equivalent to half the entire circuit. In health the half- 
circuit is completed in from twelve to sixteen seconds, much less 
time being required after muscular effort, deep breathing and the 
inhalation of nitrite of amyl. 

Fellner 3 believes that the rapidity of flow may be estimated by 
measuring with a stop-watch the length of time required for the 



1 Hemodynamisehe Studien, Berlin, 1909. 

2 The Determination of the Rate of Blood-flow Through an Organ, Reported 
at the Seventh International Physiological Congress, August, 1907. (Brodie esti- 
mated the blood-flow in an organ by suddenly occluding its peripheral vein and 
measuring the change of volume by means of an oncometer.) 

3 The Rate of Blood-flow in the Arm, Heart, i, 87. 

4 Eine klinische Methode z. Schiitzung d. Kreislaufzeit, Munch, med. Woch., 
1912, fix, 1486. 

6 Das Pulsometer, ein prakt. Instrument z. Bestimmung d. Stromgeschwindig- 
keit des Blutes am lebenden Menschen, Deut. med. Woch., 1907, Xo. 15. 



METHODS OF ESTIMATING THE RATE OF BLOOD-FLOW 171 

blood to reach the fingers — travel 50 cm. — after the release of 
tension in a pneumatic cuff applied to an arm previously rendered 
bloodless by bandaging. This method is open to many criticisms. 
(1) The air escapes from the cuff too gradually. (2) The vessels 
have been previously emptied and therefore do not offer the natural 
resistance to the flow. (3) The blood-path from the brachial to 
the digital arteries is not direct, owing to the branching and steady 
diminution in caliber of the arterial tree. 




Fig. 76. — Hewlett and Van Zwaluwenburg's method for estimating the rate of 
blood-flow. Diagram of apparatus for determining the rate of blood-flow through 
the arm. The arm is placed in the plethysmograph P, the opening of which is closed 
by a piece of rubber dam D, and the connection with the skin made tight with 
soapsuds. The narrow pressure cuff C is placed around the arm about 3 cm. 
above the opening into the plethysmograph. The pressure cuff is inflated by opening 
the stopcock connecting it with the large bottle A, in which the pressure has pre- 
viously been raised by the rubber bulb, B. Pressures are read by the spring man- 
ometer M. The plethysmograph is connected with the volume recorder V, which 
writes upon a moving drum. Air can be let out of the system by the stopcock X, 
and water can be introduced from the burette Y, so that the writing-point of the 
volume recorder can be adjusted at will. The stopcock Z serves to disconnect the 
plethysmograph from the recording apparatus during adjustments of the former. 
The recording apparatus is graduated by allowing 5 c.c. of fluid at a time to flow 
in from the burette, and marking the elevation of the volume recorder thus produced. 

The Tachograph. — The blood-flow in the arm may also be estimated 
by means of a sensitive flame. Von Kries's instrument, devised 
for this purpose, is known as the tachograph. 1 "The foreann is 
inserted into an air-tight glass cylinder, but in this case no water 
is introduced. With each svstole of the heart a certain amount of 



1 Ein Neues Verfahren zur Beobachtung der Wellenbewegung des Blutes, Berlin, 
klin. Woch., 1887, p. 589. 



172 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

air is forced out of the cylinder through the rubber tubing into a 
specially devised gasoline burner. The expelled air causes the 




Fig. 77. — The tachograph of von Kries: A, cuff; B, sensitive flame; C, camera. 




Fig. 71S. — Tachogram after von Kries. 





Fig. 79. — a, central tachogram, reading from right to left, a, at rest; b. after 
exercise. (Miiller and Veiel.) 



gasoline flame to flare upward to a height proportional to the amount 
of air displaced. This flame is in turn photographed upon a revolv- 
ing strip of paper sensitized with bromide of silver. When the 



METHODS OF ESTIMATING THE RATE OF BLOOD-FLOW 173 

tracing is developed it presents a succession of zigzags at first 
glance resembling the results of the electrocardiogram" (Fig. 77). 

When the arm increases in volume during the ventricular systole, 
the enclosed air, meeting with no resistance to outflow through 
the tubing will emerge the more rapidly and suddenly the more 
quickly the blood is forced into the arm (Figs. 78, 79, and 80). 

The Estimation of Resistance in the Large Vessels. — Brocking 1 
made brachial blood-pressure observations in the following postures : 
A, recumbent; B, sitting in bed with the legs extended; C, sitting 
with the legs dependent; D, standing. 

Normally, the pressure is highest in B, which he explains as 
due to a compensatory peripheral contraction instituted to prevent 





a b 

Fig. SO. — a, central tachogram in aortic insufficiency; b, peripheral tachogram in 
aortic obstruction. 



splanchnic anemia. It is further increased by pressing the legs 
against the abdomen. If there be circulatory weakness, the maxi- 
mum pressure in B is lower than in A , showing a loss of peripheral 
arterial' power. 

The Estimation of Arterial Functionation. — 0. Muller employs the 
following method: The arm is introduced into a plethysmograph 
and ice is applied to the arm above the instrument. Normal arteries 
show a distinct diminution, and, upon withdrawal of the cold, an 
increase in volume. In sclerotic arteries these changes are in 
part or entirely lacking. This test, although for the most part 
corroborated by other investigators, has also been criticised. 

1 Ein Beitrag zur Funktionspriifung der Arterien, Zeit. f. exp. path. u. Ther., 1907, 
iv, Pt. I. 



174 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

Cold contracts and heat dilates the arteries of healthy people 
but the psychic state also plays a considerable part. It is therefore 
necessary to arrange plethysmographic examinations in such a 
manner that thermic and psychic influences shall not be separated. 
Even if after repeated trials the vessels do not react one cannot on 
that account diagnosticate an anatomic lesion. One cannot con- 
clude that a man is arteriosclerotic because his vessels do not 
react to ice, because many organic cardiac maladies do not give 
this response, but merely that his arterial functionation is not 
normal. In the majority of individuals hardened arteries are 
hyporeactional, or even areactional to ice, although some of them 
are hyperreactional. 1 

The Estimation of Vascular Tonus. — De Vries-Reilingh 2 suggests 
the following method for determining the degree of arterial tonus: 




Fig. 81. — A, kymograph; B, plethysmograph of Mosso; B', plethysmograph of 
Wiersma; C, cuff ; D, manometer; E, pump; F, escapement; a, tambour with pen; 
b, escapement; c, occlusive rubber cuff; d, stopcock; e, three-way glass tubing. 



A small cuff is applied to the arm while the forearm is placed 
in a plethysmograph. Pressure is suddenly raised above the systolic 
pressure in the upper cuff. The tambour of the plethysmograph 
now registers a straight line; but as soon as pressure in the cuff 
falls sufficiently to allow blood to pass through, the tambour will 
rise. The pressure at this point is the maximum arterial pressure 
plus the arterial tonus. If pressure is gradually lowered a further 
rise of the tambour due to venous stagnation will occur. But in 
time a point will be reached at which the tambour falls because 
the cuff pressure has become less than the venous pressure. The 
difference in pressure between the first elevation and the first fall 
of the tambour is taken as the index of vascular resistance. This 

1 Romberg, V., and Miiller, O., Ueber d. Bedeutung u. Technik d. Plethysphyg- 
mographischen Funktionspriifung gesunder u. kranken Arterien, Zeitschr. f. klin. 
Med., 1912, lxxv, 92. 

2 Zur Blutdruckmessung, Zeit. f. klin. Med., 1913, Ixxvii, 67. 






METHODS OF ESTIMATING THE RATE OF BLOOD FLOW 17.") 

factor was found to range between 17 and 32 mm. Hg., the normal 
average being 18 mm. A source of error lies in the fact that during 
this prolonged procedure for some reason a general increase of 
pressure occurs. This rise of pressure renders an estimation of the 
minimal pressure unreliable, and while such a rise may be obviated 
by placing the cuff at the distal end of the forearm, a new source 
of error is thus introduced by the protected position of the arteries 
at this point. The results would probably also vary according to 
the rate at which the cuff pressure was lowered (Fig. 81). 

The Estimation of Capillary Blood-pressure. — Various and for the 
most part unsatisfactory methods of measuring capillary pressure 
have been suggested (see page 140). We have had no personal 
experience with the determination of the capillary tension, but it 
is manifest that if a method can be devised which is both accurate 
and clinically applicable much valuable information will be 
obtained. Simultaneous observations on the relationship between 
the arterial and the venous pressures yield more important data 
regarding the state of the circulation than either alone, since the 
arterial represents the beginning and the venous the end of the 
greater circulation. 

Combined Observations. — A more accurate though clinically 
inapplicable method of functional diagnosis originally described 
by Marey and lately rejuvenated by 0. Miiller, Romberg, and F. 
Kraus, consists of: 

1. Prolonged continuous observation of the systolic and diastolic 
pressures. 

2. Continuous tachographic observation undertaken simultane- 
ously with the foregoing. 

If both pressure and rate increase it is assumed that we are 
dealing with an increased systolic output; if the two values move 
in opposite directions, that an alteration of peripheral resistance in 
the arm under observation has occurred. 

3. Plethysmography observations to determine vascular changes 
in the arm. 

But even this method does not permit us to draw deductions 
which can be expressed in actual figures. 

The Sphygmobolometer. — This instrument devised by Sahli 1 is 
used to estimate the energy of individual puhe waces, and thus 
indirectly the energy of cardiac systole. 

1 Sahli's Diagnostic Methods, 1911, p. 1S6. 



176 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

The Principle. — The pulse wave is made to transmit its force to 
a measured quantity of air enclosed in a cuff (A) encircling the 
forearm and communicating with a manometer. The pressure 
in the cuff is raised until the maximum oscillation occurs in the 
oscillator (d), this point being known as the optimum pressure. 



/=H 



U 




Fig. 82. — Schematic diagram of Sahli's sphygmo bolometer: A, cuff; 6, inflating 
bulb; C, mercurial manometer; E, graduated piston pump; d, index manometer. 
Lower diagrams: A, lateral view of the steel cuff; E, index manometer in horizontal 
and erect position. 



This is accomplished through the use of a steel outer cuff, with 
which tension can be very exactly regulated and the precise point 
noted at which the maximum oscillation is overstepped. 

The energy of that portion of the aortic wave which reaches the 
brachial artery is expended in three directions: (1) That which 



METHODS OF ESTIMATING THE RATE OF BLOOD-FLOW 177 

passes the cuff. (2) That which is reflected backward toward the 
heart. (3) That which compresses the cuff. Manifestly only the 
latter portion can be measured, thus ever leaving two undetermin- 
able factors. 

By observing the actual height of the manometric pressure which 
corresponds to the optimum pressure, by noting the extent of 
oscillation of the latter, and knowing the volume of the enclosed 
air we are enabled to construct a formula which represents the 
amount of energy expended. The volume of air is measured by 
means of a graduated piston syringe (E) with a capacity of 200 c.c. 
The cubic capacity of the index manometer is determined for each 
individual instrument, the lumen being calibrated in such a manner 
that each centimeter of length is equivalent to 0.02 c.c. The 
instrument is based upon Boyle's (Mariotte's) law that if tem- 
perature remains constant the volume of gas will vary inversely as 
the pressure, whence follows the formula: 



w 



= v {bTp) {bTp) (Ap)13 - 6 



W = work performed by each pulse wave. 
V = volume of air. 
(A p) = maximum oscillation reduced to cm. Hg. 

B = mean barometric pressure = 76.4 (New York). 

P = pressure in cm. Hg. at maximum excursion of index manometer. 



F = ^~. -„- -— -^ 13.6 



B \ 


( P 


B +Pj 


\B +P 


P. 


F. 


5 


0.78 


6 


0.92 


7 


1.04 


8 


1.16 


9 


1.28 


10 


1.39 


11 


1.49 


12 


1.59 


13 


1.69 


14 


1.78 


15 


1.87 


16 


1.95 


17 


2.02 


18 


2.10 


19 


2.17 


20 


2.23 


21 


2.30 


22 


2.36 


23 


2.42 



12 



178 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

A table can be worked out so that each estimation requires but 
one multiplication: (A p) X (F X V). 

The accuracy of any single determination depends mainly on 
the reading of (A p), errors in the other terms being negligible in 
comparison. Thi sinvolves a reading of the excursions of the 
kerosene index and a calibration of these excursions in terms of 
mercury. Computations show that under normal conditions results 
obtained by an experienced observer can be relied on to better 
than 10 per cent. (Potter). 1 




Fig. 83. — The sphygmobolometer. The rubber bag D is applied over the radial 
artery by the cuff H and connects by means of tubing with the (1) 10 c.c. syringe 
G and (2) with the index manometer EF, which contains colored kerosene and 
(3) with the vertical mercury manometer A. (Sahli.) 

"The value of B in a given locality may be assumed to be 
constant, as may also the volume V for a given instrument. A 
similar table would have to be worked out for each individual 
instrument. 

W = F X V X (A p) 

"The total work of the pulse per minute is obtained by multiply- 
ing the work of a single beat by the pulse rate. We are of course 
not measuring the entire energy of the heart but only that fraction 



1 Jour. Amer. Med. Assn., April 19, 1913, p. 1211. 






METHODS OF ESTIMATING THE RATE OF BLOOD-FLOW 179 

of it which is consumed in furnishing the pulse wave in the brachial 
cuff — this Sahli believes to be a constant fraction." 1 

The most recent modification of sphygmobolometry 2 consists 
in the substitution of a Jacquet sphygmograph equipped with a 
spiral spring in place of a pneumatic cuff. The coefficient of 
elasticity of the spring is practically constant for different pressures, 
hence it is possible to take the arithmetic mean of the beginning 
and end tension of the pressure. In order to translate the spring 
tension into grams the apparatus is equipped with a device to draw 
upon the smoked paper nine parallel abscissae. For each of these 
abscissae, the pressure value of the spring is established in grams 
and tabulated. These abscissae indicate the height of the pelotte 
plus the magnification due to the tambour. Thus it is possible 
to take tracings of different degrees of spring pressure, choosing 
those as our criteria which yield the largest work product. Needless 
to say, a sphygmograph must be applied with accuracy and care. 

Dynamic Diagrams. — T. F. Christen suggests the use of "dynamic 
diagrams" 3 as an index of cardiac work, a conception which he 
bases on the following hypothesis: 

The Theory. — The old-fashioned palpation of the pulse tells 'us 
much more about the condition of the circulation than does the 
sphygmogram, in spite of the latter's seemingly higher scientific 
character. In the clinical sphygmogram there is no exact relation 
between the ordinates and the pressures. We do not even know 
where to trace the level of the pressure zero. Even if there were 
such a relation, sphygmography would still not be a dynamic method, 
as in dynamics we do not have to study alone the temporal variations 
of the forces, but essentially the effect of these forces. These two 
statements sufficiently explain the failure of the clinical sphygmo- 
gram. There are two dynamic diagrams of the pulse that may be 
determined in a mathematically exact manner. They are the 



'For more detailed discussion see Sahli, Deutsch. med. Woch., 1907, No. 16, 
p. 628; No. 17, p. 665. Sahli, Diagnostic Methods, edited by Potter, W. B. Saunders 
Company, Philadelphia, 2d Ed. Sahli, Deutsch. med. Woch., 1910, No. 47, p. 2181. 
Christen, Zeitsch. f. klin. Med., 1910, lxxi, 390. Sahli, Zeitsch. f. klin. Med., 1911, 
lxxii, 1. Sahli, Zeitsch. f. klin. Med., 1911, lxxii, 214. Christen, Zeitsch. f. klin. 
Med., 1911, Ixxiii, 55. Christen, Deutsch. med. Woch., 1911, No. 14, p. 644. Chris- 
ten, Cor. Bl. f. schweiz. Aerzte, 1911, p. 562. Sahli, Zeitsch. f. klin. Med., 1912, 
lxxiv, 230. Christen, Zeitsch. f. klin. Med., 1912, lxxiv, 447. 

2 Lipowetsky, L., Sphygmobolometrische Untersuchungen an Gesunden und 
Kranken mittels des Sahlischen sphygmobolographischen Verfahrens, Deutsch. 
Arch. f. klin. Med., 1913, cix, S. 498-514. 

3 Die neuen Methoden d. Dynamischen Pulsdiagnostik, Zeit. f. klin. Med., 1911, 
Ixxviii, 55. 



ISO FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

graphic expression of clinical experiments based upon the following 
two questions: (a) What is the systolic increase of volume of the 
arteries covered by a pneumatic cuff by a given pressure? (6) 
What is the amount of mechanical energy required for this move- 
ment? These dynamic diagrams, called stasis curves, are char- 
acteristic of the behavior of the pulse against a stasis pressure. 
They depend on the volume of air within the cuff as little as they 
do on the elasticity of the cuff and the soft parts. They depend 
only on the breadth of the cuff. We, therefore, have to compare 
stasis curves derived from experiments with cuffs of the same 
breadth. The exclusive consideration of pressure and its temporal 
variations will never permit us to solve the question of diagnosis 
of the pulse, for the mechanics of the pulse contain essentially 
dynamic problems more than any other province of physiology. 
The stasis curves (dynamic diagrams) replace the palpation of 
the pulse by an exact method, because they answer the same 
questions that palpation does, informing us concerning the "filling" 
and the "intensity" of the pulse. The method depends on the 
estimation of the force necessary to produce the oscillations which 
are observed in the determination of the pulse-pressure. This 
variation in the volume of the artery does not depend on the volume 
of air within the cuff, nor on the elasticity of the system. It can 
depend only on pressure exerted by the inflated cuff and on the 
dynamic qualities of the pulse. 

The Method. — In order to find the value of the systolic increase 
of Volume, i. e., the volume of blood the pushing forth of which 
against the pressure of the cuff produces the oscillations observed 
on the manometer, we make use of a syringe whose piston has 
to be pushed in up to the point where the oscillations have been 
displaced about once their own amplitude. 

Example. — We observe on the manometer oscillations between 

the limits 170 and 176. (The unit of the manometer is prjrr 2 -) 

Pushing in the piston of the syringe we increase the pressure within 
the cuff, elevating both limits of these oscillations. We do this in 
such a manner as just to reach the point where 176 has become 
the lower limit of the oscillations, having been heretofore its upper 
limit. Thus we are sure that the volume of the piston, which is 
read off on its own scale, must be that incompressible volume 
which brought under the cuff increases the pressure within it from 
170 to 176. Two incompressible volumes, which, forced into the 



METHODS OF ESTIMATING THE RATE OF BLOOD-FLOW 181 

same air-chamber produce the same increase of pressure within it, 
must be equal. Therefore, the volume read off and the piston 
must be equal to the systolic increase of volume of the artery (or 
arteries) that is covered by the inflated cuff. Suppose that we 





























































































































































































































^ 






























V=2.0cm s 








































































1 




























/ 


/ ' 
































/ 






































\ 




\ 


















i 


/ 
•> 
























) 














\ 




\ 


















/ 


























A 4 - 














\ 




\ 




1.5 






































/■ 
















\ 






v 












/ 
























/ 


















\ 






\, 












1 


























/ 




































/ 


























/ 




























































V 




























1.0 


































A 


























































/ 




\s> 
























































y 






\ 


i. 


















































^ 


a 








\ 




























- 


















i 


s 


S 














\ 
























0.5 














y- 


<fc 


















\ 


































\^ 


A 




// 




\ 
















1 
































/ 


S 






f 








\ 
















\ 




























Y 






/ 


■? 










V 














\ 






























Y 


s 


/ 












I 




























































T 





































■ 50 



100 



150 



200 



2.50 



300 



350 



Fig. 84. — Dynamic diagrams. Curve of volume: 1, that of health; 2, of myo- 
carditis; 3, of aortic insufficiency; 4. of arteriosclerosis. In cases of forcible pulsa- 
tion — arteriosclerosis, aortic insufficiency — the volumes may exceed 2 cm. and the 
energy 600 gr. cm. Furthermore, the character of the summit is quite different 
from that of arteriosclerosis. 

read a volume of 0.7 cm., then the mechanical energy required for 
the same increase of volume — the main pressure being: 



gr. gr. 

173 /SVT 2 — must have the value 173 p.., X 0.7 cm. : 



121 gr. cm. 



In this way we find for every pressure (P) a volume (V) and an 
energy (E), the relation between which is E = PV. Repeating 
this experiment at different pressures we get a series of pressure 
volumes and energies which we arrange in the following manner: 



182 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 



Energy. 
8 

36 

77 
149 
228 
252 
203 

90 

50 



Diagrams. — In order to give a clearer idea of the relation between 
these quantities, viz., pressures, volume, and energy, we plot two 
curves which represent the volumes or the energies as functions 





Example 


Pressure. 


Volume. 


80 


0.1 


120 


0.3 


140 


0.55 


165 


0.9 


190 


1.2 


210 


1.2 


225 


0.9 


240 


0.4 


250 


0.2 




Fig. 85. — Christen's energometer. 



of the pressure. Therefore, in our graphic method we have to plot 
the pressure as abscissae and the volumes or the energies as ordi- 
nates. The author employed the leg instead of the arm for these 
determinations, because he found that in cases of hypertension 
disagreeable sensations and even pain may be produced, an occur- 
rence which it is said can be avoided when the cuff is fastened 
around the calf (Fig. 84). 



METHODS OF ESTIMATING THE RATE OF BLOOD-FLOW 183 

We have had no experience with Christen's method. The author 

claims that the results obtained by it when applied in studying 

the effect of work, rest, medication, etc., are satisfactory. It is 

essential that the variations of the summit — a rise or a fall, a 

shifting to a higher or lower level, a sharpening or flattening of 

the curve (Fig. 84) be expressed in absolute values — the pressure 

gr. 
in f^nr 2 , the volume in cm. and the energy in gr. cm. 1 

Extreme care in technique is absolutely essential. The readings 
must be taken with the patient as well as the patient's arm in the 
same position. The cuff must be applied to exactly the same region 
of the arm, which should be marked, and needless to say the same 
arm must be used for successive observations (Dunkan). Leg 
readings are inaccurate. The energy of the pulse wave even in 




Fig. 86. — Engelen's instrument for the determination of intra-abdominal pressure. 

normal subjects is variable, but there are limits which are not 
normally exceeded. Muscular exercise, and cardiac hypertrophy 
with good compensation show high readings. Adrenalin injections 
cause high values independently of any effect on blood-pressure 
(Drouven). 

The Determination of Intra-abdominal Pressure. — Blood-pressure 
may be considerably influenced by intra-abdominal pressure, on 
which account it is sometimes desirable to know what the height 
of the latter pressure is. This may be determined (1), as suggested 
by Moritz, by introducing into the stomach a tube into which a 
thin rubber window has been inserted, the tube being connected 

1 Christen's energometer, manufactured by Hausmann Instrument Company, 
St. Gallen, Switzerland. 



184 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

with a monometer. (2) By means of a special instrument devised 
by Engelen 1 which consists of a large glass bell, the bottom of which 
is sealed with thin rubber dam. The latter will project either 
inward or outward, as the pressure relations on either side of the 
membrane may vary. 

The instrument is placed upon the abdominal wall, connected 
with a manometer, and sufficient air is pumped into the bell to 
equalize the pressure on each side of the membrane in the interior 
of the bell and the outer abdominal wall — this being shown by an 
indicator. 

Deep insiration may cause a pressure of — 57 mm. Hg.; forced 
expiration, +87 mm. During normal parturition a pressure of 40 
mm. is usual which with dystocia may rise as high as +125 mm. 

(3) Variations in abdominal pressure may also be determined by 
inserting a rubber bag (cylinder in casts 7 cm. by 16 cm.) into the 
rectum, which when inflated with air is connected with a Marey 
tambour. 2 The normal intra-abdominal pressure is above that 
of the atmospheric pressure. It fluctuates with the respiratory 
excursions of the thorax and the diaphragm. Anything which 
diminishes the tone of these structures causes a lowering of abdom- 
inal pressure. Distention of the abdomen by fluid or gas increases 
the pressure and this is in turn followed by a fall of blood-pressure 
due to a diminished venous inflow, and consequently a decreased 
left ventricular systolic output 3 (see page 41). 

1 Ueber Messung u. Bedeutung des Abdominaldruckes, Deut. med. Woch., 1911, 
No. 19. 

2 Weber, E., Ueber eine neue Methode zur Untersuchung der Drucksehwank- 
ungen in der Bauch Hohle, Zentralbl. f. Physiol., Leipsic u. Wien, 1900. xx. 329-336. 

3 Emerson, H., Intra-abdominal Pressure, Arch. Int. Med., 1911, vii, 3.54. 



CHAPTER VI. 
ARTERIAL HYPOTENSION. 

ESSENTIAL HYPOTENSION (CONSTITUTIONAL LOW 
ARTERIAL PRESSURE). 

Arterial hypotension, by which we understand a systolic 
pressure of or below 115 mm. Hg., generally in association with a 
diastolic pressure below 80 mm., is a very common condition. 
Hypotension may occur after hemorrhage, in acute infectious dis- 
eases, in conditions of malnutrition or cachexia, such as tuber- 
culosis, carcinoma, Addison's disease. It may also occur in anemia, 
in paresis, in osteo-arthritis, in cardiac dilatation, tachycardia and 
in cardiac decompensation. Two renal conditions — cyclic and 
orthostatic albuminuria, and amyloid disease of the kidney are 
often associated with low blood-pressure. It may also occur as a 
result of intoxication — anaphylaxis, nicotinism, alcoholism. Hypo- 
tension also occurs in surgical shock; as a result of some forms of 
anesthesia, especially that of chloroform, and as a terminal event 
during the last ebbing time of life. 

Relative hypotension often follows hypertension when vascular 
and cardiac resources are overtaxed. 

Arterial hypotension may occur in: (1) Acute infectious disease. 
(2) Chronic malnutrition, with or without toxemia. (3) Certain 
individuals in whom the condition or a marked tendency toward 
it appears to be a part of their constitutional make up. (4) In 
association with abnormalities of the endocrine functions of the 
male gonads. 

Symptomatology. — Essential hypotension is a very common 
condition, the importance of which has been signally emphasized 
by L. F. Bishop. Many apparently healthy individuals, although 
not robust, often in youth and early adult life normally have a 
systolic and a diastolic blood-pressure ranging between 115 and 100, 
and between 80 and 70 mm. respectively. Such individuals lack 
stamina, tire easily, complain of cold extremities and of the inability 
to do prolonged mental or physical work. They often suffer from 



186 ARTERIAL HYPOTENSION 

dyspepsia, which upon investigation proves to be of the "nervous" 
variety, not infrequently due to hypomotility and superimposed 
on an anatomical background of partial or total splanchnoptosis. 
They are not actually ill, yet they are rarely well; they complain 
of all sorts of symptoms, headache, lassitude, mental depression, 
"gouty" pains, constipation, etc. Their bodily temperature is 
generally subnormal in the morning and they suffer from cold 
extremities due to a sluggish peripheral circulation. They are apt 
to be filed away in that much overloaded diagnostic pigeon-hole 
labeled "neurasthenia." They are often of the high-strung nervous 
temperament, "go on their nerves," are moody and emotional, 
and sensitive to caffein and nicotine, as well as to atmospheric and 
barometric fluctuations. Staehelin 1 found that a fall of barometric 
pressure produces a lowering of the arterial tension in many indi- 
viduals. In extreme cases they often fall asleep when sitting 
upright and suffer from insomnia when they go to bed. Perhaps 
enough has been said to illustrate the picture, although pages might 
be written upon the symptomatology. 

The inability of the subjects of constitutional hypotension to 
stand the demands of prolonged physical exertion is the direct 
result of their low blood-pressure. Recent experimental evidence 
has shown that an increased arterial pressure such as occurs normally 
during exercise increases the height of muscular contraction when 
the pressure is below a certain critical level, whereas a decreased 
pressure below this point has the opposite effect. An increased 
flow flushes out and neutralizes the fatigue products. 2 

Observations over a period of two years in a case of constitutional 
low tension by Edgecombe 3 showed that pressure was higher in the 
evenings than in the mornings. No relationship could be estab- 
lished between pressure and pulse rate. Exercise, mental effort, 
grief, altitude, tea, coffee, and tobacco had a pressure-increasing 
effect. Constipation lowered the tension. Therapeutically, caffein 
and pituitary substance raised, whereas alcohol lowered the pressure. 
Strychnin, digitalis, calcium, and glycogen were without effect. 

While it is unsafe to generalize from a single case, the results 
reported correspond quite closely to what is usually observed in 
this class of cases. 



1 Ueber d. Einfluss d. taglichen Luftdruckschwankungen auf den Blutdruck, Med. 
Klinik, 1913, ix, 862. 

2 Gruber, C. M., Studies in Fatigue, Amer. Jour. Physiol., 1913, xxxii, 221. 

3 Royal Soc. Med., Med. Sect., February 28, 1911. 



ESSENTIAL HYPOTENSION 187 

Patients with essential hypotension not only have an habitually 
low blood-pressure, but their response to different stimuli which 
normally affect blood-pressure either locally or generally is either 
quantitatively or qualitatively abnormal. The effect of a change 
of posture from the recumbent to the erect position is normally a 
variable one, but the maximum and minimum pressures invariably 
approach each other (Erlanger). The pulse rate decreases, the 
pulse pressure falls. These changes are due to the effect of gravity. 
The pressure in the femoral artery is higher than that in the carotid 
in proportion to the difference of the hydrostatic pressure of the 
column of blood which separates the two points of measurement. 

Difference in height 
of column separating 
Posture. Brachial. Tibial. Difference. armlets. 

Horizontal .... 140 138 2 

Standing .... 136 204 68 -68.5 

L. post., legs up . . 122 76 46 46.1 

Vertical, head down 148 70 78 77.7 

If normal postural change in pulse rate (6 to 10 beats) does not 
occur, it shows too miich; if exaggerated, too little splanchnic 
tone. If the response is reversed there is apt to be extensive 
disease of the cardiovascular system — generally hypertension. 
In healthy individuals the transition from the recumbent to the 
erect posture generally produces a slight fall of the systolic and 
a rise of diastolic pressure, thus a diminution of pulse pressure. 
In people with relaxed abdominal walls and enteroptosis a marked 
falling of the systolic pressure (25 mm.) and a slight lowering of 
the diastolic pressure have been noted. 1 (See Crampton's test, 
p. 146). A lowered splanchnic tone leads to more or less cerebral 
anemia, and a sudden assumption of the erect posture when the 
individual has been recumbent or stooping to the ground with the 
knees flexed often causes a temporary vertigo. Sjmcopal attacks 
from relatively insufficient causes are in case of the female sex, at 
least, by no means rare. An engorged condition of the viscera is 
often evident on inspection during abdominal operations. The 
vascular supply especially in the veins is excessive. Ptosis of the 
right kidney not only tends to constrict its own vascular supply, 
but by dragging upon the inferior vena cava and the aorta may 
seriously disturb the lumen of these vessels, contributing in no small 

1 Birtch, Fayette W., and Inman, Thos. G., Blood-pressure Observations on 
Patients with Relaxed Abdominal Musculature, Jour. Amer. Med. Assoc, 1912, 
lviii, S. 265-268. 



188 ARTERIAL HYPOTENSION 

measure to vascular stasis. 1 These results are noted clinically by the 
large gush of urine which often follows a short period of recumbency. 
(See Arterial Functionation, p. 173.) 

Another frequent symptom resulting from low blood-pressure 
is headache, relief from which is too often sought in headache 
powders, which of course eventually aggravate the condition. 
Elevation of blood-pressure is followed by improvement. 

Etiology. — "In the upright posture the blood tends to settle 
in the capacious channels of the splanchnic vascular bed. The 
'head-up' position in four-footed animals may lead to extraor- 
dinary lowering of blood-pressure in the carotid arteries and 
presumably to critical anemia of the brain. But in man there 
has been developed a compensatory reaction, undoubtedly chiefly 
vasomotor, by means of which the vessels of the dependent parts 
of the body, probably the arteries of the splanchnic area, contract 
under stimulus of the upright posture and maintain a fairly uniform 
distribution of the blood-mass. 

"No physiologic coordination can be conceived that is more 
important than this to the welfare of the organism as a whole. 
It is to be expected, therefore, on a priori grounds, that minor 
compensations having the same general purpose should here and 
there disclose themselves. When the radial pulse fails in a wrist 
which is raised above the level of the head, the result may be due 
either to passive drainage of the blood from the artery, followed 
by a purely local contraction of the arterial wall, or to active vaso- 
motor contraction of the vessel under the stimulus of gravity. As 
touching the former view, Bayliss has shown that peripheral 
arteries freed from their nervous connections respond to variations 
of internal pressure by contracting as the pressure rises and dilating 
as it falls. Sifting the great number of observations bearing on 
this subject, the latter explanation seems to be the only possible 
one. In other words, according to this view pulse failure in the 
elevated radial artery is a sign of vasomotor activity and belongs 
to the series of physiological compensations. It is comprehensible 
as such, if we presume that contraction of the radial arteries helps 
to maintain blood-pressure in more vital tissues by diverting the 
blood-stream from less sensitive organs. It has often been observed 
that pulse failure which is obvious in the elevated wrist at the 
beginning of a series of observations is not evident later on. That 

1 Mackenzie, K. A. J., The Role of Movable Kidney in Intestinal ami Vascular 
Stasis, Jour. Amer. Med. Assn., 1912, lix, 33S. 



ESSEN TI. 1 L II YPOTENSION 189 

is, the pulse failure mechanism seems subject to fatigue. Excitement 
or emotion which increases the total outflow of nerve energy tends 
to inhibit the pulse failure. In general, in perfectly normal in- 
dividuals who are in vigorous physical condition, the radial pulse is 
maintained when the arms are raised. In the same class of persons, 
when more or less debilitated by confining occupations or sub- 
nutrition, the pulse often fails. In an acute febrile disorder the 
pulse usually remains when the arms are raised; during convales- 
cence, especially with the establishment of compensation in cardiac- 
disease, the pulse often fails. Numerous observations seem to show 
that these differences in the reaction of the pulse do not depend on 
the amount of blood volume or the degree of maximal arterial 
pressure. It is not only conceivable, but probable, that signs of 
physiologic compensation which are absent during robust health 
or active disease should become manifest when the normal vital 
energy is reduced or when, as a result of disease, the efforts of 
physiologic adjustment must become more strenuous to maintain 
the needful outflow and normal distribution of the blood-mass. 
The older writers in this field were prone to attribute the pulsus 
paradoxus to mechanical interference with the normal blood-flow, 
basing their position on the frequency with which the phenomenon 
attends pathologic adhesions between the mediastinal tissues. The 
facts that have been rehearsed seem to indicate that mechanical 
abnormalities within the chest may only indirectly cause pulse 
failure, by exaggerating certain reflexes which under perfectly 
normal conditions are masked. 

"As already stated, failure of the elevated pulse does not seem 
to occur in persons showing signs of general arteriosclerosis. The 
thought may not be far amiss that this constant organic tendency 
of later life may in itself be a compensation which, by diminishing 
the distensibility of the vessels under the hydrostatic pressure of 
the blood, may more or less substitute that constant and necessary 
redistribution of the blood-mass which has become impossible to 
a senile vasomotor apparatus" (L. Hill). 

Goldthwaite 1 classifies the essential hypotensive individual as the 
" carnivorous type" of man and suggests that the low blood-pressure, 
weak pulse, subnormal matutinal temperature, etc., are due to 
mechanical causes. According to this conception the absence of 
retroperitoneal fat exposes the sympathetic ganglia and the large 

1 Shattuek Lecture, An Anatomic and Mechanistic Conception of Disease, Boston 
Med. and Surg. Jour., 1915, clxxii, 881. 



190 ARTERIAL HYPOTENSION 

bloodvessels which lie unprotected on the anterior surface of the 
spine, to irritation and pressure except when the individual lies 
on his face or his side. This perhaps also applies to the adrenals. 
A long mesentery by dragging downward in the erect posture 
favors splanchnic stasis; and the low diaphragm with its small 
respiratory excursion does not efficiently aid the propulsion of 
blood from the abdominal to the thoracic cavity. While these 
anatomical factors perhaps cannot alone account for the symptoms, 
they are quite sufficient to do so when we add the faulty standing 
and sitting postures which are habitually assumed by individuals 
of this type. 

The most constant finding in the class of individuals under 
consideration is arterial hypotension. They often have varying 
degrees of gastroptosis but so do many apparently healthy people 
whose blood-pressure is normal and who have no gastric symptoms 
so long as their nerve tone is up to par. It would seem, therefore, 
that the splanchnoptosis is not the underlying causative factor, 
although it unquestionably acts an important part in some cases. 
We further ask ourselves whether the hypotension is the cause of 
the nervous manifestations or whether a lack of proper nervous 
stimuli is the cause of the hypotension? This question cannot be 
positively answered. Undoubtedly there is a complex interaction 
of these causes by virtue of which the one may deleteriously affect 
the other, from which we could readily construct a beautiful and 
typical example of the "vicious circle" did it seem worth while to 
do so. 

Chronic low arterial pressure has also been attributed to toxemia, 
and cholin salts have been suggested as the active substance. 1 It 
has been claimed by Popielski and Modrokowski that chemically 
pure cholin would produce a rise, not a fall of pressure, but Mendel, 
Underhill and Renshaw 2 have shown that the injection of chemically 
pure cholin did produce a short fall of pressure. 

Functional or constitutional physiologic vasomotor unfitness, 
owing mainly to improper nerve balance, seems to be the most 
satisfactory explanation for the majority of cases of afebrile hypo- 
tension. 

1 Morel, Albert, Recherches sur l'origine clinique de l'hypotension, Livre jubilaire 
du Pr. Teissier. Lyon, 1910. 

2 Action of Salts of Cholin on Arterial Blood-pressure, Jour. Phar. and Esp. 
Therap., 1912, iii, 649. 



ORTHOSTATIC ALBUMINURIA 191 

ORTHOSTATIC ALBUMINURIA. 

In health the assumption of the erect posture produces an 
increased urinary flow, and a relatively increased sodium chloride 
output. In the subjects of circulatory disease the conditions are 
reversed. In orthostatic albuminuria there is a qualitative change 
which points to a less efficient renal circulation in the standing- 
posture. 1 

Numerous observers have commented upon the frequent associa- 
tion of orthostatic albuminuria and cardiovascular weakness. 
This form of albuminuria is often associated with arterial hypo- 
tension. The thought naturally suggests itself that the albuminuria 
is brought about by the fact that the splanchnic vasomotor ap- 
paratus only insufficiently compensates the blood-pressure changes 
induced by a change of posture, thus leading to vascular changes in 
the kidney and the albuminuria while the patient is erect. 2 The 
exact nature and mechanism of these vascular changes is still in 
doubt. Renal anemia or venous congestion, either as the result of 
increased intra-abdominal pressure or from kinking of the vessels 
in a more or less movable kidney, have been suggested. 

Neither of these explanations is universally applicable. The 
kidneys are by no means always movable, and increase of intra- 
abdominal pressure on standing occurs in normal individuals. 
Further, why should the albuminuria only appear on rising in 
the morning and not in the afternoon? According to Porges and 
Pribram, 3 the cause lies in a spastic contraction of the renal arteries. 

This type of albuminuria is sometimes seen in convalescence, 
either from fevers or from trauma, which has necessitated a long 
stay in bed, under which conditions the vasomotor response to 
changes of posture are soon lost, so that the individual on assuming 
the erect posture promptly becomes weak and dizzy. 

Hooker found that with a constant mean pressure the rate of 
blood-flow and of urinary secretion bear a direct relation to the 
pulse pressure, whereas the albumin secreted by the kidney varied 
inversely, experimental evidence which is in accord with the findings 
of Erlanger and Hooker in two cases of orthostatic albuminuria. 4 

1 Loeb, H., Klin. Untersuch. ii. d. Einfluss von Kreislaufsaenderungen auf d. 
Urinzusammensetzung, Deut. Arch. f. klin. Med., 1905, lxxxiv, 579. 

2 Muntzer, E., Zur Lehre v. d. vaskularen Hypotonien, Wien. klin. Woch., 1910, 
xxiii, 1341. 

3 Zur Kentniss d. orthostatischen Albuminurie, Deut. Arch. f. klin. Med., 1907, 
xc, 367. 

1 Jour. Physiol., November 1, 1910. 



192 ARTERIAL HYPOTENSION 

Recent researches of Bass and Wessler 1 have, however, contro- 
verted a number of the previously described results. They found 
that blood-pressures in children suffering from orthostatic al- 
buminuria differ but little from normal findings. 

"Functional" albuminuria is not infrequently met with at the 
period of adolescence, often in association with anemia and low 
blood-pressure. Dukes, who has observed many of these cases 
classifies them in three categories. 

1. Cases with cold extremities, clammy hands, low blood-pressure, 
and deficient vasomotor reactions, as shown by syncopal attacks, 
and by a fall of blood-pressure upon rising from a reclining to an 
erect posture. 

2. Cases with very labile but generally high blood-pressures. 
This is the commonest type. 

3. Cases occurring in spare, neurotic, high strung and generally 
hyperesthetic individuals. 

It is of course well known that posture may affect albuminuria 
even in organic cases, especially those associated with cardiac 
insufficiency. 

The significance of albuminuria may often be more correctly 
interpreted by means of blood-pressure observations. This symp- 
tom may occur in perfectly healthy young men after forcible 
exercise. In association with slight hematuria it is especially fre- 
quent after boxing bouts, in which "kidney blows" abet its appear- 
ance (Stanton). The occurrence of albuminuria after strenuous 
exercise is generally attributed to a secondary splanchnic vasodila- 
tation which follows the primary vasoconstriction, and which 
produces a temporary renal congestion. Paroxysmal hemoglo- 
binuria and hematuria have also been attributed to loss of 
vasomotor equilibrium. Hemoglobinuria is sometimes brought on 
by walking, especially if this is done in a lordotic posture. This 
type of hemoglobinuria has been explained as resulting from vaso- 
motor instability causing an abnormal circulatory state in the 
spleen. 2 

. ARTHRITIC AND RHEUMATOID CONDITIONS. 

Excluding lesions of a true gouty nature which are usually 
associated with hypertension, there is a large group of so-called 

1 Blood-pressure in Children Showing Orthostatic Albuminuria, Arch. Int. Med., 
1913, xiii, 39. 

■ Porges and Strisower, Deutsch. Arch. f. klin. Med., January 7, 1915, No. 2. 



ARTHRITIC AND RHEUMATOID CONDITIONS 193 

"rheumatic" ailments whose pathogenesis is still unknown, which 
often occurs in hypotensive individuals and which tends to disappear 
when, as the result of a more efficient circulation, better nutrition 
of the muscles, joints and fibrous structures has been obtained. 
To this class belong certain cases of lumbago, sciatica, neuritis, 
stiff neck, and "myalgia." Rheumatoid arthritis and "phospha- 
turia" also generally occur in association with low arterial pressure. 

Low blood-pressure is also met with in cases of status lymphaticus 
in which condition, according to Wiesel 1 and Hedinger, 2 it is asso- 
ciated with hypoplasia of the chromaffin system. 

Treatment of Essential Hypotension. — The curvative results of 
therapy in arterial hypotension are never brilliant and often dis- 
appointing, and yet in the majority of cases, especially if the subject 
be not too far advanced in life, much can be accomplished. The 
trouble lies in the fact that we are combating an inbred constitutional 
weakness and that an arrest of symptoms often only lasts as long 
as the treatment is continued. 

The treatment consists mainly in a proper regulation of the 
patient's daily life, the details of which must be supervised with 
the idea of diminishing the factors which lead to a lowered nerve 
tone. That mental overwork is often largely contributory in 
increasing hypotension is corroborated by Bonser's 3 studies, which 
showed that intellectual fatigue among twelve students observed 
was capable of diminishing vasomotor reactions to emotional 
stimulation. A complete rest cure in extreme cases may be advisable 
at the beginning. After this a general routine mode of life as is 
generally advised for neurasthenic patients is in order. A few 
points, however, deserve to be emphasized: (1) Requisite rest and 
sleep (an eight-hour allowance of the latter being a minimum). 
(2) Relaxation — the avoidance of too prolonged mental or physical 
work. The necessity of a small but regular amount of physical 
exercise, preferably outdoor. (3) The avoidance of excesses — 
dietary or sexual. (4) Tobacco — these patients are very sensitive 
to tobacco, an excessive use of which is often directly accountable 
for their symptoms. 

Hydrotherapy. — Aside from the foregoing, hydrotherapy is by 
far the most successful method of treatment. The Nauheim bath, 

1 Zur Path. d. chromaffinen System, Virchow's Archiv., 1904, clxxvi. 

2 Ueber d. Kombination von Morbus Addisonii mit Status Lymphaticus, Frank- 
furter Zeitsch. f. Path., 1907, i, 527. 

3 Psych. Rev., March, 1903. 

13 



194 ARTERIAL HYPOTENSION 

the Vichy douche 1 or the needle bath may be recommended, but 
almost equally good results may be obtained with the ordinary 
home shower bath. 

The patient is instructed to take a hot tub bath each morning 
on rising, practising active autofriction with rough linen tape wash 
rags or mittens. When thoroughly warmed he is to turn on the 
cold shower, this to be followed by active friction with a rough 
towel. The length of the stay under the cold spray is to be gradually 
increased and after a short trial will be attended by a good vigorous 
reaction, the skin becoming pink and accompanied by a pleasant 
tingling glow. This treatment must be kept up indefinitely. Where 
no shower bath is available, cold water may be poured over the 
head and shoulders from pitchers. 

In patients with enteroptosis and with relaxed abdominal muscles 
systematic exercises, calculated to restore muscular tone, or some 
form of abdominal support, are of distinct utility. Massage is 
also beneficial. 

Goodman 2 has emphasized the importance of daily morning 
calisthenics, especially those which tend to compress the abdominal 
viscera, increase respiratory excursion and strengthen the muscles 
which maintain a correct standing posture. Such exercises must 
not be carried to the point of breathlessness, much less exhaustion, 
but should be gradually increased in severity and duration as the 
individual is trained up to his task. 

Drugs. — Strychin as an adjuvant to increase nerve tone is the 
most generally useful drug, though it has no direct effect on blood- 
pressure. Digitalis is useless unless there be a definite cardiac lesion. 

Although we possess numerous drugs which may be used to lower 
blood-pressure, few if any fulfil the purpose of raising blood-pressure. 
Watson 3 found that atropin, camphor, cotarnin, digitoxin and 
strychnin were valueless for this purpose. Physostigmin, which 
may raise pressure, cannot be used in adequate dosage on account 
of nausea and vomiting. Tyramin (said to be the most important 
active constituent of the watery extracts of ergot) gave better 
results. Musser, Jr., has reported good results following the 
administration of pituitrin (see p. 340). 

1 The Vichy douche consists of a needle douche projected downward on the patient 
throughout the duration of the bath, while general massage is administered by an 
attendant. 

2 Some Cases of Arterial Hypotension Associated with a Definite Symptomatology, 
Am. Jour. Med. Sci., 1914, cxlvii, 503. 

3 The Value of Drugs as Blood-pressure Elevators, Practitioner, 1915, xciv. No. 4. 



ARTHRITIC AND RHEUMATOID CONDITIONS 195 

Termination.— The ultimate outcome of cases of essential hypo- 
tension has, so far as we are aware, not been studied. Individuals 
belonging to this class are of necessity seriously handicapped in 
their career. They cannot, as a rule, lead the strenuous life which 
seems, in this country at least, to be fast becoming the "normal." 
But whether this enforced moderation leads to a longer life, with 
a diminished tendency toward the development of arteriosclerotic 
changes, is an interesting question. If our interpretation of the 
pathology of this condition is correct, the splanchnic vessels are 
habitually relaxed and overloaded with blood. Does such a condi- 
tion predispose to vascular disease of the intra-abdominal vessels 
and organs, or does the passive overloading with venous stasis 
exert a less deleterious effect upon the vascular wall than an active 
distention due to a powerful heart and a high vascular tonus? 
Do these individuals later in life develop arterial hypertension as 
the result of splanchnic arteriosclerosis with its attendant dangers 
and discomfitures, or does Nature mitigate these tendencies as a 
compensation of earlier disabilities? These questions must await 
further studies before an answer can be given. The case of the 
puny dyspeptic "weakling" who weathers the storm of an acute 
infection to which the robust "full-blooded" athlete succumbs is 
well known, as is also the lanky dyspeptic who outlives his plethoric 
friends. " Causa latet, res ipse notissima." 



CHAPTER VII. 
BLOOD-PRESSURE IN ACUTE INFECTIOUS DISEASE. 

Practically all infectious fevers are accompanied by a fall of 
blood-pressure, although in some, this feature is specially marked. 
The personal equation of the patient of course greatly influences 
the result. In the so-called sthenic fevers blood-pressure is not 
much affected. In asthenic fevers the fall is very pronounced. 
Many of the ill effects of fever are directly due to low arterial 
pressure and it is now generally admitted that death in many 
infections, is quite as much due to vasomotor as to cardiac failure. 
A few microbic toxins (Staphylococcus, pyocyaneus, mallein) 
seem to have hypertensive qualities (Bosc and Vedel). 

Broadly speaking, the extent of pressure fall tends to vary 
directly with the fever, but there are many exceptions to this rule, 
for the reason that the pressure is influenced more by the toxemia 
than by the pyrexia. In severe infections with a weakening circula- 
tion the systolic pressure falls and pulse pressure decreases. A well- 
sustained pulse pressure is to be construed as a favorable sign. 

Degeneration of the adrenal glands in infections, especially 
diphtheria, and the experimental production of similar lesions by 
toxin injections have led some authors to recommend adrenalin 
as a therapeutic medium, both on account of its effect in raising 
blood-pressure, and on account of an hypothetic protective power 
in the defense of the organism. 

In 11 cases of infectious disease, Marx 1 found no lack of epinephrin 
in the blood, nor was the blood-pressure especially low. The amount 
of epinephrin recoverable from the suprarenal glands after death 
bears no relation to the character of the fatal disease. The height 
of blood-pressure bears no relation to the epinephrin content of 
the glands. The variable results are perhaps due to the gradual 
death of different sets of the glandular cells. It seems likely, 
therefore, that the beneficial effect of epinephrin in shock and 
allied states is due to its vasoconstrictor action. It is therefore 

1 Ueher den Adrenalingehalt der Nebennierne, Med. Klinik d. Stadt. Krankenanst, 
Mannheim, Dissert. Heidelberg, 1912, xxiv. 



BLOOD-PRESSURE IN ACUTE INFECTIOUS DISEASE 107 

merely a symptomatic and not a specific means of therapeusis. 
Elliot, 1 on the other hand, found that the store of epinephrin in the 
adrenal glands is diminished by fright, anesthesia, cerebral injury 
and bacterial intoxications. The residual epinephrin has been 
found especially low after death from pneumonia, although dimin- 
ished amounts were also found after measles, scarlatina, acute 
febrile tuberculosis, malignant endocarditis. Since the adrenal 
glands are not considered responsible for the normal maintenance of 
blood-pressure, but are regarded as emergency organs, this would 
indicate that in order to combat the hypotension entailed by these 
infectious processes the adrenals had been called upon for a reserve 
supply, and showed a corresponding exhaustion. The decrease of 
residual epinephrin encountered was never sufficient to account for 
circulatory failure. 

During the height of continuous fevers, blood-floic at the periphery 
is somewhat slower than in health. The conditions are quite dif- 
ferent than when bodily temperature is artificially raised by the 
external application of heat. In the latter case, as w r as shown 
by Hewlett 2 and Van Zwaluwenburg, the peripheral circulation is 
enormously increased, just as it is when a person sweats owing to 
the high temperature of a room. In fevers the vessels still dilate 
under the influence of external heat, but the heightened tempera- 
ture of the body does not influence the heat regulatory mechanism 
in such a way as to cause their dilatation. The experimental 
researches of Newburgh and Lawrence 3 indicate that, in lower 
animals degrees of hyperthermia not greater than those encountered 
in infections are sufficient to cause marked hypotension. The 
increased body temperature of infection is a potent factor in the 
production of the lowered blood-pressure which occurs in such 
conditions. The hyperthermia may be the entire cause of such 
hypotension. A temporary rise of pressure sometimes accompanies 
the outbreak of the rash in the exanthemata — scarlatina, morbili, 
variola, etc. 4 The work of the heart is increased during fever if 
the blood-pressure remains constant. 5 



1 Pathologic Changes in the Adrenal Glands, Quart. Jour. Med., 1914, viii, No. 29, 

2 The Effect of Room Temperature upon the Blood-flow in the Arm, etc., Heart. 
ii, 230. 

3 The Effect of Heat on Blood-pressure, Arch. Int. Med., 1914, xiii, 287. 

4 Weigert, K., Verhalten d. art. Blutdrucks bei akuten Infektionskrankheiten, 
Volkmann's Samml. klin. Vortr., 1907, No. 459; Inn. Med., cxxxviii, 6.5. 

'■ Wolf, H. F., The Influence of Temperature on the Output of the Heart, Arch. 
Int. Med., 1911, viii, 463. 



198 BLOOD-PRESSURE IN ACUTE INFECTIOUS DISEASE 

Convalescence from prolonged fevers is attended by a loss of 
splanchnic tone, in part due to depressed nervous influence and 
in part to weakening of the arterial musculature. When the patient 
assumes the erect posture there is a marked falling of the maximal 
pressure, even when the minimal pressure remains unchanged. 
This diminishes the pulse pressure, as a result of which the deficiency 
of cerebral blood-supply must be compensated for by an increased 
pulse rate, which throws an unnecessary strain on the heart. This 
condition is often associated with cardiac murmurs, accentuations, 
reduplications or arhythmia. Minor degrees of physical exertion 
may cause a fall of 30 to 40 mm. Hg. Under such conditions the 
patient should not be allowed to leave his bed so long as there is a 
marked difference in pulse rate between the erect and the recumbent 
postures. Cardiac erythism and vasomotor instability are often 
encountered. 

As elsewhere actual figures are of little value. It is the course of 
the pressure, upward or downward, or marked lability, which is 
of importance. For this reason pressure readings should be made 
and charted simultaneously with the temperature. Marked fluc- 
tuations in the height of the systolic pressure are of serious import. 
Many of the older reports on blood-pressure in infectious disease 
are practically useless because they record only the systolic pressures, 
and even these were often made with unreliable instruments. 

The fact is generally recognized that practically any infection 
may produce cardiovascular damage. Thayer found that individuals 
who had passed through attacks of typhoid fever showed a dis- 
proportionately higher pressure in later life than those who have 
not had this disease. The lesson is obvious: that convalescents 
should be spared all unnecessary activity for prolonged periods of 
time. Schwartzmann's 1 recent studies lead him to conclude that 
in infectious diseases a high diastolic pressure indicates a tendency 
to splanchnic stasis — a severe infection. A fall of both systolic and 
diastolic pressure points to vasomotor weakness, whereas a fall of 
the systolic, associated with a rise of the diastolic pressure shows 
cardiac failure. 

The venom pressure tends to fall with the arterial pressure in 
infectious disease, but when cardiac failure begins venous pressure 
rises. 

1 Klinische Bedeutung der Feststellung d. systolischen u. diastolischen Blutdruck 
bei Iufektionskrankheiten, Zeitsch. f. inn. Med., 1914, xxxv, 745. 



ACUTE INFECTIONS 199 

ACUTE INFECTIONS. 

Cholera. — In this disease the specific gravity of the blood may 
rise to 1060 to 1070, due to loss of fluid, and systolic blood-pressures 
as low as 70 mm. Hg are not rare. 

In the algid stage, according to Lang, 1 the pulse pressure decreases 
owing to a fall of the maximum and a rise of the minimum pressures. 
Diastolic pressure diminishes only in severe cases. These changes 
are due to loss of the liquid constituents of the blood and to 
consequent vasoconstriction. Saline transfusions averaging 2 liters 
are generally sufficient to restore the total volume of blood and 
bring the pressure relations back to the normal. Larger trans- 
fusions often lead to supernormal values as the hypertonicity of 
the vascular system tends to continue for some time and the pulse 
rate to rise. Following the algid stage and during the "typhoid" 
stage an increased blood-pressure is the rule. 

The blood-pressure is therefore a satisfactory criterion of the 
amount of saline infusion to be administered. When given in too 
large quantities an unnecessary amount of work is thrown upon the 
heart. The judicious employment of saline infusion with epi- 
nephrin has in one epidemic at least greatly lowered the mortality 
of cholera. 2 During the recent epidemic in Serbia vaccine was 
administered in large doses of physiologic salt solution with definitely 
beneficial results. 

Diphtheria. — Cardiovascular disturbances occur in about 10 
per cent, of all diphtheria cases. Death is due to (1) the effect 
of the toxin on the vasomotor centre, heart, and adrenals; (2) to 
myocardial lesions (chiefly parenchymatous; (3) to involvement 
of the stimulus conducting system; (4) to bronchopneumonic 
manifestations. 3 

Experimental Data. — The experimental injection of diphtheria 
toxin does not always cause an immediate fall of blood-pressure. 
Such a fall occurs some time after the injection of cultures and 
appears suddenly. 4 Romberg and Paessler showed that in the 

1 Ueber den arteriellen Druck bei Cholera asiatica u. s. Veraendrungen unter d. 
Eiiifluss grosser Kocbsaltzinfusionen, Deut. Arch. f. klin. Med., 1912, eviii, 236. 

2 Rogers, L., A Second Season's Experience of Hypertonic Transfusions in Cholera, 
Controlled by Observations on the Blood Changes, Therap. Gazette, November, 
1909, xxxiii, 761. 

3 Leede, W. H., Beitr. z. Diphth. mit besonderer Berucksichtigung d. path, anat., 
Organ u. bacteriologischen Leichenblutbefunde und ihrem Verhalten zum klinischen 
Bilde. (3671 cases), Zeit. f. klin. Med., 1913, lxxvii, 297. 

J Beck and Slapa, Ueber d. Einfluss d. Diphtheriegiftes a. d. Kreislauf, Wien. klin. 
Woch., 1S9.5, xviii. 



200 BLOOD-PRESSURE IN ACUTE INFECTIOUS DISEASE 

early stages at least the hypotension was vasomotor in origin, but 
von Slejskall was able to show a direct toxic action upon the heart. 
Lethal doses of diphtheria toxin after a latent period of twenty-four 
hours produce a marked fall of pressure up to the point at which 
death occurs. The timely injection of antitoxin delays this fall 
of pressure and in sufficient dosage prevents death, but even in 
excessive dosage fails to restore a pressure which has already fallen 
dangerously low. 1 MacCallum's 2 experiments indicate that the 
death which occurs at the height of an attack of diphtheria is not 
exclusively the result of direct cardiac injury, although that may 
have a part in the process. Porter and Pratt 3 found that even in 
the late stages of lethal diphtheria intoxication the vasomotor 
centre still responds to both pressor and depressor stimuli, showing 
that death is not primarily due to vasomotor paralysis. Myers 
and Wallace 4 have shown that although the larger bloodvessels in 
intoxicated animals responded normally, the arterioles and capil- 
laries in the splanchnic domain fail to react normally to epinephrin 
and are found in an engorged condition. It appears, therefore, 
that peripheral splanchnic paralysis accounts for the hypotension 
of diphtheria. 

Clinical Data. — Diphtheria is accompanied by low arterial tension, 
the degree of which often stands in proportion to the severity of 
the attack. The highest readings occur in the first and the lowest 
in the second week of the disease, normal tension being reestablished 
by the seventh week. Laryngeal cases, especially those requiring 
operation, show a higher pressure as a result of asphyxia. Trache- 
otomy is often followed by a sudden fall (20 to 40 mm.). Pressure 
in the early stages is ordinarily not much affected by serotherapy; 
in the latter stages it may rise 40 per cent. In cases manifesting 
anaphylactic phenomena there is a great fall of pressure (see page 210) . 

Circulatory weakness is a prominent feature of the disease, and 
the normal postural blood-pressure changes are often absent or 
reversed even during convalescence. 5 The onset of nephritis is 
not always accompanied by an increase in blood-pressure. 

1 Meyer, Fr., Beitr. z. Kenntnis d. Diphtherievergiftung, etc.. Arch. f. exp. Phar., 
1909, No. 60. 

2 The Mechanism of Circulatory Failure in Diphtheria, Amer. Jour. Med. Sci., 
1914, cxlvii, 37. 

3 The State of the Vasomotor Centre in Diphtheria Intoxication. Amer. Jour. 
Physiol., xxxiii, 431. 

4 The Vascular Response in Poisoning from Diphtheria Toxin, Proc. Soc. Exper. 
Biol, and Med., 1914, xii, 43. 

6 Rolleston, J. D., Blood-pressure in Diphtheria, British Jour. Children's Dis., 
October, 1911, viii, 28. 



ACUTE INFECTIONS 201 

There is no fixed relation between fever and blood-pressure. 
The fall of the latter is due to the absorption of toxins, as shown 
by animal experiments. The most marked fall in pressure occurs 
in those cases in which antitoxin treatment has been delayed. 
When the fall of pressure is marked there is usually more or less 
cardiac involvement. Intravenous saline injection sometimes 
produces temporary inprovement, probably by diluting the toxins. 1 
A fall of pressure after an amelioration of acute symptoms is often 
the first sign of persistent toxemia. 2 

Fatal cases sometimes show a marked fall of pressure several 
days before the lethal termination. A progressive fall of tension is 
of bad prognostic import, as is also a unilateral pressure difference, 
but high pressure does not of necessity presage a recovery. 

As a means of differential diagnosis between true diphtheria 
and simulating infections, blood-pressure readings are valueless. 
The occurrence of paralysis is sometimes preceded by a fall of 
pressure (Kolossova). 

Malaria. — According to Federn, blood-pressure rises during the 
chill and falls during the period of sudation. In chronic malarial 
cachexia, hypotension is the rule. 

If some of the recent hypotheses regarding malaria, which are 
based upon facts discovered since the artificial cultivation of the 
Plasmodium has become possible, should prove true, blood-pressure 
may have a more important bearing upon malaria than has been 
supposed. It has been suggested that after attaining a certain 
size the plasmodium reaches and lodges in the capillaries and that 
in this situation the inoculation of new corpuscles normally takes 
place. The debris and pigment which result from their destruc- 
tion may, if the infection be severe, "plug" the brain capillaries 
and produce "cerebral malaria." Further, the height of the blood- 
pressure and the state of capillary dilatation or constriction would 
influence the stage at which the organisms would recede from the 
peripheral blood-stream into the capillaries to undergo segmenta- 
tion, or destruction, or to invade new T blood-cells. At this point, 
too, the organisms would be immune to the effects of quinine which, 
according to this view, is not directly toxic but merely increases the 
permeability of the red cell to the normal destructive serum. 3 

1 Cobliner, W., Blutdruckmessungen bei erwachsenen Diphtheriekranken, Dissert., 
Berlin, 1912, p. 45. 

2 Schoen, C, Deut. med. Woch., March 27, 1913. 

3 Jour. Amer. Med. Assoc., 1914, lxii, 1330. 



202 BLOOD-PRESSURE IN ACUTE INFECTIOUS DISEASE 

Meningitis. — Epidemic cerebrospinal meningitis is almost con- 
stantly associated with high intracranial tension. Moderately 
increased blood-pressure is not infrequntly seen in the early acute 
stage, during exacerbations of. symptoms late in the disease, or 
where the malady assumes a chronic aspect. Often the higher 
the pressure the more severe the case. The withdrawal of cerebro- 
spinal fluid by lumbar puncture, while usually attended with a 
fall, has no constant effect on blood-pressure. It seems, therefore, 
that increased intracranial tension in meningitis does not necessarily 
cause a rise of blood-pressure unless it be late in the disease, when 
internal hydrocephalus may develop as a result of blocking the 
foramina of the fourth ventricle. 1 

Tuberculous Meningitis. — In tuberculous meningitis arterial 
pressure is but slightly elevated, the readings obtained are about 
normal; whereas, in tuberculous disease they are generally sub- 
normal. In other forms of meningitis very high pressures are 
sometimes encountered (230 mm.) which sometimes tend to run a 
parallel course with the increased pressure of the cerebrospinal 
fluid. 2 

Since meningitis is sometimes treated by intraspinal injections 
it is important to know how high the intraspinal pressure may 
be raised without danger. It has been found experimentally that 
although there is a marked difference in sensitiveness in different 
individuals, a sudden increase of pressure is always more dangerous 
than a gradual one. The first mechanical effect is upon the 
respiratory centre, followed quickly by profound cardiac inhibition 
which causes a sudden and tremendous fall of blood-pressure. 
Inasmuch as this is not a vasomotor disturbance, epinephrin is 
not indicated. In fact it would probably do harm on account of 
its cardiac inhibitive effect. 3 The best results are obtained through 
the use of cocain and atropin, the former stimulating the respiratory 
centre and the latter lessening cardiac inhibition. (See Lumbar 
Puncture.) 

Pneumonia. — The view that death from pneumonia frequently 
results from peripheral vasomotor paralysis has been quite generally 
held, despite the fact that clinical observations are not at all unani- 

1 Robinson, G. C, Blood-pressure in Cerebrospinal Meningitis, Arch. Int. Med., 
May, 1910, p. 482. 

2 Parisot, J., La pression arterielle dans les meningites, Soc. Med. de Nancy, 
December 8, 1909; Rev. Med. de l'Est, 1910, p. 48. 

3 Carter, W. S., The Effect of Intraspinal Injections of Ringer's Solution in Differ- 
ent Amounts under Varying Pressures, Arch. Int. Med., 1912, x, 42.">. 



ACUTE INFECTIONS 203 

mous in supporting this view. Among 19 fatal cases, and 2G eases 
which recovered, Newburgh and Minot found that the systolic- 
pressure in the fatal cases was continuously above that in the 
cases which recovered. In 1899 Romberg and his associates 
endeavored to test the state of the vasomotor mechanism by the 
use of stimuli to the skin and mucous membranes. After producing 
a fatal pneumococcus septicemia in rabbits, blood-pressure was 
observed in the animals after electrical stimulation applied to the 
nasal and anal mucous membranes. In the early stages of the dis- 
ease sensory stimuli always caused a marked elevation of blood- 
pressure. At a later period, when the appearance of the animals 
suggested the approach of death and the temperature was falling, 
the reflexes were still present but did not attain the normal height. 
Finally, when the animal was in a state of collapse and death was 
imminent no rise of blood-pressure followed peripheral stimulation. 
As a result of their observations, Romberg and his co-workers 
believed that they had proved that death in acute infectious diseases 
was the direct outcome of paralysis of the vasomotor centre in the 
medulla. 

This, it is to be observed, is an experiment of a negative sort, 
since it rests entirely upon failure to obtain certain physiological 
responses. 

Porter and Newburgh 1 have recently completed experiments 
from which they obtained positive information regarding this 
problem. 

They produced not only pneumococcic septicemia in rabbits, 
but also acute fatal pneumonia in rabbits, cats and dogs. In order 
to judge of the condition of the vasomotor apparatus, they measured 
the vasomotor reflex. But instead of using precarious reflexes 
from the mucous membranes, Porter and Newburgh exposed and 
cut the depressor and the sciatic nerves and stimulated the central 
ends. 

The data obtained are probably more reliable than those first 
mentioned, since the depressor nerve is composed entirely of fibers 
which affect the vasomotor centres, whereas other nerves contain 
fibers of widely different function. As a result of these symptoms 
they found that the vasomotor centre was not impaired in any of the 
examples of fatal pneumonia studied. 

It is not surprising, therefore, that low blood-pressure in pneu- 

1 The State of the Vasomotor Apparatus in Pneumonia, Am. Jour. Physiol., 1914, 
xxxv, 1. 



204 BLOOD-PRESSURE IN ACUTE INFECTIOUS DISEASE 

monia is not invariably of evil omen, indeed the systolic pressure 
is often higher in fatal than in non-fatal cases, and hence Gibson's 
rule is far from infallible. The rate of the pulse and not the blood- 
pressure level, is the chief factor in deciding whether the pressure 
will or will not fall below the pulse. 1 

On the other hand, as opposing the view that pneumonic death 
is primarily a cardiac failure, it has been shown that: (1) The heart 
muscle is not functionally impaired in pneumonia since the pneu- 
monic ventricle beats normally as soon as its food is normal; (2) 
pneumonic blood, suddenly fed to a normal heart muscle, lowers its 
efficiency, lessening the duration and the area of contraction; (3) 
the heart muscle in pneumonia gradually exposed to the action of 
the poison, largely adjusts itself to its poisoned food. 2 Death in 
pneumonia is often attended with the same symptoms as those 
produced by surgical "shock." There is often no dilatation or 
engorgement of the right heart. In lobar pneumonia there is, in 
addition to hypotension, the added mechanical obstruction in the 
lungs with which the right heart has to cope. Pulmonary involve- 
ment is often extensive, but experiments have demonstrated that 
one-sixth of the total lung capacity is sufficient to maintain life, 3 
and in the advanced stages of tuberculosis an individual often lives 
for weeks or months with very little lung tissue intact. It is not, 
therefore, the extent of the pulmonary lesion which is of primary 
importance in pneumonia but the degree of toxemia, and this is 
often reflected in blood-pressure estimations. Such readings should 
be made routinely in all cases. 

As first discovered by Gibson, the ratio of pulse rate and blood- 
pressure may be of some prognostic value. "A pressure appre- 
ciably below the normal in pneumonia is invariably of evil omen, 
and any considerably fall bodes disaster. When the arterial pressure, 
expressed in millimeters of mercury, does not fall below the pulse 
rate expressed in beats per minute, the fact may be taken as of 
excellent augury, while the converse is equally true." This state- 
ment has found corroboration from many sources. 4 

The pulse-pressure ratio must not be accepted too literally; 

1 Newburgh and Minot, Arch. Int. Med., 1914, xiv, 48; Newburgh, Am. Jour. 
Med. Sci., February, 1915, p. 204. 

2 Newburgh, L. H., and Porter, W. T.. The Heart Muscle in Pneumonia, Jour. 
Exper. Med., 1915, xxii, 123. 

3 Bernard, L., Le Play, Mantoux, C, Capaeite pulmonairc minima compatible 
avec la vie, Jour, de physiol. Exper., 1913, xv, 16. 

■"Goodman and Pitman, Therap. Gazette, July 15, 1911. 



ACUTE INFECTIONS 205 

for individuals who have habitually a high pressure may, when 
critically ill, show a more favorable ratio than their condition 
justifies. On the other hand, patients with essential hypotension 
may show a lower pressure while their actual- condition may be 
quite satisfactory. Howell 1 has found that in doubtful cases 
observation of the relative intensity and duration of the first four 
auscultatory phases may be distinctly helpful. Strong, clear- 
cut sounds over an artery are indications of circulatory strength. 
This applies specially to the third phase, in pneumonia. 

" More is to be gained from watching the changes in a succession 
of sequences than from isolated observations, for, indeed, one 
patient may be quite comfortable with a sequence which in another 
promises the worst." In pneumonia the persistence of the second 
phase, which is most readily lost, is of favorable import. All 
clear tapping sounds are of good augury, whether heard in that 
part of the sequence usually assigned to the third phase or not, 
whereas feeble, muffled sounds must be considered as unfavorable. 
"When the clear tap is lost and the sequence appears as a succes- 
sion of dull, muffled sounds from systole downward, a high grade 
of peripheral relaxation and secondary cardiac exhaustion can be 
inferred. When to this arhythmia is added, the worst picture is 
drawn." 

Venous pressure is low, but rises as cardiac weakness increases. 

The beneficial effect of cold fresh air are unquestionable, but 
they cannot be explained as the result of any direct effect upon 
blood-pressure. A slight rise of systolic pressure of variable dura- 
tion is produced in normal adults by exposure of the face to cold 
air, but is often followed by a fall to the original level even while 
the exposure is continued. 2 Van Ordt, 3 it is true, found a slight 
rise of blood-pressure following exposure to cold, but not greater 
in amount than the normal physiologic range. Barringer obtained 
practically negative results, regardless of whether the entire body 
or only the face was exposed. 

Scarlet Fever. — The fall of pressure, which occurs in about 25 
per cent, of the cases, 4 is less than in typhoid fever, and stands 

1 Possibilities in the Use of the Auscultatory Method of Determining Blood- 
pressure in Pneumonia, Jour. Amer. Med: Assn., 1914, lxii, 1230. 

2 Barringer, T. B., The Effect of Cold Air upon the Circulation in Healthy and 
Sick Individuals, Amer. Jour. Med. Sci., 1912, cxliv, 233. 

3 Zeit. f. Dial. u. physik. Therap., 1905, ix, 338. 

4 Rolleston, J. D., The Blood-pressure in Scarlet Fever, British Jour. Child. Dis., 
1912, ix, 444. 



206 BLOOD-PRESSURE IN ACUTE INFECTIOUS DISEASE 

in direct relation to the severity of the attack. It appears during 
the period of eruption and is pronounced during febrile deferves- 
cence. In mild cases pressure is but slightly affected. In grave 
cases a marked fall -is associated with a high temperature and a rapid 
pulse. The normal is gradually reestablished during convalescence, 
more slowly after severe cases. Slight albuminuria may not be 
accompanied by a rise of pressure. 1 In scarlatinal nephritis, 
blood-pressure sometimes rises before albumin has appeared in 
the urine. Cardiac involvement is sometimes associated with a 
slight rise and marked lability of arterial pressure (Weigert). 
Dietary modifications — milk, salt, salt-free food — and minor 
complications have but little effect on blood-pressure. 2 

Smallpox. — The pustulation stage is associated with a fall of 
arterial pressure which compares in degree to the toxemia. A 
return to the normal during convalescence occurs very slowly. 3 

Typhoid and Paratyphoid Fever. — The blood-pressure in typhoid 
fever falls below the normal after the patient takes to his bed and 
remains low until convalescence is established. This is the result 
of toxic vasomotor depression. The fall of pressure bears no 
constant relation to the pulse or temperature curve or the severity 
of the attack, but a rapid or progressive fall of pressure is often of 
serious augury. The value of blood-pressure readings as a means 
of differential diagnosis or prognosis is not of much value. 4 

Both systolic and diastolic pressure fall during the later febrile 
period, and rise coincidently at the beginning of the afebrile period. 
Later on in convalescence the systolic and diastolic levels move 
farther and farther apart, owing either to a systolic rise and a 
diastolic fall or because the one pressure remains stationary while 
the other recedes from it. Finally, sometimes suddenly and at 
times coincidently with leaving bed, both pressures attain a higher 
level. Studies of the "pulse-pressure quotient" and the "amplitude 
frequency product" indicate that during the febrile period the 
heart performs increased work despite the lowered pressure, and 
that circulatory weakness is in part cardiac and in part vasomotor 
in origin. Further, that in one case which came to autopsy, 

1 Teissier and Tanon, Le Pression arterielle dans la Scarlatine de l'Adulte, Jour. 
Physiol, et. Path. Generale, 1908, x, 481. 

2 Nobecourt and Teissier, La Pression arterielle dans la Scarlatine de l'Adulte, Jour. 
Physiol, et. Path. Generale, 1908, x, 481. 

3 Davidson, Blood-pressure in Fevers, Lancet, October 19, 1907. 

1 Weigert, K., Ueber d. Verhalten d. arteriellen Blutdrucks bei d. akuten Infek- 
tionskrankheiten, Samml. klin. Vortrage, 1907, xvi, No. 9. 



ACUTE INFECTIONS 



207 



toxemia was accountable for the condition, since no microscopic 
myocardial lesions were encountered (Fig. 87). l 



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Fig. 87. — Record of a rapidly fatal case of typhoid fever in which death apparently 
resulted from cardiac weakness. The systolic pressure falls, the diastolic pressure 
rises, the quotient and the amplitude frequency product steadily decline, while the 
venous pressure and the pulse rate rise. Microscopic examination of the heart being 
negative death was ascribed to toxic factors. (Dietschy and Hossli.) 



In 115 cases the average pressure was found to be: First week, 
115 mm.; second, 106 mm.; third, 102 mm.; fourth, 96 mm.; fifth, 

1 Dietschy, R., and Hossli, H., Beitrage z. Beurteilung d. Kreislaufsverhaeltnisse 
bei Infektionskrankheiten, etc., Deut. med. Woch., April 24, 1908, xciii. 



208 BLOOD-PRESSURE IN ACUTE INFECTIOUS DISEASE 

98 mm. The occurrence of perforation is often followed within two 
to four hours by a rise of from 20 to 70 mm. It is caused by (a) 
pain, and (b) beginning peritonitis, in the early stages of which 
condition a marked pressure increase is often seen. 1 In the later 
stages a toxic paralysis of the vasomotor and respiratory centres 
in the medulla occurs (Romberg and Heineke). 

In cases of relapse, the pressure which may have risen during 
the afebrile period undergoes a second drop, often to a still lower 
level. These changes may precede the rise in temperature. 

During convalescence there is a slow, gradual rise of pressure 
(sometimes interrupted by temporary drops), which increases 




Fig. 88. — a, maximum pressure; 6, minimum pressure; c, temperature; d, pulse 
rate; c, blood-pressure quotient; /, pressure of the jugular vein. 



more rapidly when the patient is again up and about. Hemorrhage 
is usually followed by a fall, sometimes a marked fall, of pressure 
(20 to 40 mm.). In cardiac weakness, marked diurnal variations 
may occur. 

Cold sponging raises the pressure 10 to 15 mm. in cases which 
respond favorably to the treatment; in the cases which become 
cyanotic, this rise does not occur. A complicating pneumonia 
may temporarily raise the pressure, as may also the psychic effect 
of too many visitors. 2 To be of any value in typhoid fever blood- 
pressure observations should be made twice daily. The normal 

1 Crile, G. W., The Diagnostic Value of Blood-pressure Observations in the Diag- 
nosis of Typhoid Perforation, Jour. Amer. Med. Assn., 1903, xl, 1292. 

2 Barach, Blood-pressure in Typhoid Fever, New York Med. Jour., August 24, 1907. 



ACUTE INFECTIONS 209 

individual range will then be reestablished and changes definitely 
demonstrated. If perforation is anticipated readings should be 
made at half-hourly intervals. 

Treatment. — Hypotension per se is not a symptom calling for 
treatment any more than is hypertension. The resting body can 
do with a pressure well below the normal without deleterious 
effects; indeed, this may be a method of conserving energy. Only 
when pressure falls progressively or is accompanied by other signs 
of cardiac or vasomotor failure is interference warranted. Many 
a case of typhoid fever or pneumonia weathers the attack satis- 
factorily, having a systolic pressure of about 100 mm. Hg., without 
stimulation. 

When, however, a falling pressure is associated with an increased 
pulse rate, pallor, sweating, cold extremities, and other signs of 
collapse, direct treatment, calculated to restore vasomotor tone, 
is indicated. It is generally easier to keep up pressure by early 
treatment — sponging, etc. — than to restore it once it has fallen 
to the danger limit. The best results will usually be obtained by 
fresh air, cold sponging, saline enteroclysis, or intravenous infusion. 
The addition of from 0.5 to 1 per cent, of sodium bicarbonate to 
the 0.8 per cent, sodium chloride solution is advisable. The addition 
of the former salt produces a greater rise of the diastolic pressure 
and seems to exert a definitely stimulating effect upon the heart 1 
(see page 382). In the course of fever the peripheral circulation, as 
indicated by the flow of blood in the foot, is distinctly subnormal. 
This apparently results from vasoconstriction, an effort on the 
part of Nature to secure an increased blood -flow for the organs 
chiefly involved. According to this hypothesis, fever is due to 
more rapid flow, and therefore increased metabolism of the internal 
organs. Hence, cold sponging would seem to be the most valuable 
form of treatment, since it tends to abet the natural process; 
whereas antipyretic and other vasodilator drugs are directly contra- 
indicated, since they tend to interfere with the natural mechanism 
of healing. 2 Since febrile hypotension is essentially toxic in nature, 
all available means must be employed to counteract or minimize 
toxemia. Febrile hypotension is often associated with tympanites, 



1 Dawson, The Changes in the Heart Rate and Blood-pressures Resulting from 
Severe Hemorrhages and Subsequent Infusion of Sodium Bicarbonate, Jour. Exp. 
Med., 1905, vii, 1. 

2 Stewart, G. N., Blood-flow in the Feet, with Special Referezice to Fever, Jour. 
Exp. Med., 1913, xviii, 354. 

14 



210 BLOOD-PRESSURE IN ACUTE INFECTIOUS DISEASE 

which symptom should be zealously guarded against, since it 
indicates indigestion and malnutrition, and because it seriously 
embarrasses both respiration and heart action. 

Treatment therefore should consist of (1) Combating Toxemia. 
This is to be accomplished by increasing elimination by attention 
to the emunctories. Proper evacuation of the bowels and increasing 
the urinary output are useful measures. The latter is often best 
accomplished by increasing the fluid intake by mouth, by means of 
continuous enterocylsis (drip method), by intravenous saline 
infusion or hypodermoclysis. Fresh air plays an important role. 

2. Vasomotor stimulation, by cold sponging or tubbing, or by the 
use of drugs which act upon the central or peripheral vasomotor 
system. 

The drugs most commonly employed are strychnin, atropin, 
caffein, camphor, digitalis, strophanthus, pituitrin, epinephrin. 
Although they may do good, improvement cannot, except in case 
of the last two, be attributed to direct blood-pressure raising 
qualities (see under Therapeutics). 

Medical or Toxic Shock. — A condition of shock practically 
identical with that seen after surgical trauma may occur as the 
result of anaphylaxis. The injection of foreign proteids, horse 
serum for instance, is sometimes followed by sudden collapse or 
even death from this cause. A distinction is often made between 
shock and collapse. In the former we are dealing with a lowering 
of vasomotor tone due to insufficient reflex splanchnic stimulation; 
in the latter the vasomotor paresis is due to depression resulting 
from toxemia. Pearce has shown experimentally that in both 
anaphylactic shock and in peptone intoxication in dogs there is a 
great fall of blood-pressure (20 to 30 mm. Hg.) due to splanchnic 
dilatation and resulting in medullary anemia. Cardiac and respi- 
ratory abnormalities are entirely secondary manifestations. 

Physiologic studies having for their object the determination 
of the mechanism by which the low pressure is caused, demonstrate 
that the condition is essentially a peripheral vasomotor paralysis. 
Pharmacologic studies indicate that the effect is on the nerve 
endings rather than on the muscle. 

With independent cerebral transfusion the recovery from low 
pressure is more rapid than in the intact animal. This is true also 
when an animal is transfused by carotid anastomosis, and recovery 
is especially satisfactory when the transfusion is accompanied by 
simultaneous bleeding from the femoral vein. 



THE EFFECT OF DRUGS ON THE VASOMOTOR SYSTEM 211 

The researches of Auer and Robinson 1 indicate that in animals 
at least the fall of pressure seen in anaphylactic shock may be 
partially cardiac in origin. The electrocardiogram shows variable 
abnormalities, ranging from an increased depression of the S-wave 
to complete dissociation of stimulus conduction. 

Henderson and Barringer state that "in both hemorrhage and 
circulatory shock the decrease in the venous supply to the right 
heart is the critical factor. In this they differ from vasomotor 
failure, in which the peripheral resistance of the arterial system is 
decreased." 

"The indications for treatment, therefore, appear to be' (1) relief 
of splanchnic congestion, and (2) increase of volume of blood to 
the heart and medulla. Cardiac stimulants alone, or salt solution 
and adrenalin alone, cannot bring about a permanent improvement. 
A combination, however, of the slow injection of adrenalin in salt 
solution (1 to 40,000) intravenously with the addition of a pure 
cardiac stimulant, as digitoxin, leads to relatively rapid and per- 
manent improvement, by promoting a determination of the blood 
to the right heart and increasing the circulation in the brain" 
(Pearce) . 2 

As a prophylactic measure in anaphylactic shock, the utility 
of atropin has been demonstrated by Auer. 3 In guinea-pigs with- 
out atropin, 75 per cent, died; with this drug only 28 per cent. 
(see Surgical Shock, page 378). 

THE EFFECT OF DRUGS ON THE VASOMOTOR SYSTEM. 

Strychnin, while it may be useful in other ways, does not stimulate 
the vasomotor centre except in toxic doses. 

Epinephrin has no direct effect on the centre, but may be useful 
in emergency for its sympathetic stimulation. 

Camphor is probably without effect on the centre, as is also 
spartein. Ergot increases pressure by its stimulation of the sym- 
pathetic nerve. 

The vasomotor centre is depressed by chloroform; ether 



1 An Electrocardiographic Study of the Anaphylactic Rabbit, Jour. Exp. Med., 
1913, xviii, 450. 

2 A Study of Experimental Conditions of Low Blood-pressure of Non-traumatic 
Origin, Archives of Internal Medicine, August, 1910, vi, 218; also, A Study of 
the Action of the Heart in Anaphylactic Shock in a Dog, Jour. Phar. and Exp. 
Therap., 1912, iv, No. 1. 

3 Amer. Jour. Physiol., September, 1910. 



212 BLOOD-PRESSURE IN ACUTE INFECTIOUS DISEASE 

stimulates moderately, if it has any effect. Pituitrin has but a 
slight action on the centre. It is a useful emergency measure which 
raises pressure by its action on the peripheral arterial muscle. 1 
Alcohol is deleterious if increase of pressure is the desideratum. 

If the hypotension results from cardiac weakness digitalis, or 
strophanthin may be tried, although their effects are often disap- 
pointing in febrile toxemia. An ice-bag applied to the precordium 
is often the most satisfactory method of steadying the heart. 

1 Pilcher and Sollmann, Studies on the Vasomotor Centre, Jour. Phar. and Exp. 
Therap., 1915, vi, 323. 



CHAPTER VIII. 
BLOOD-PRESSURE IN CHRONIC INFECTIOUS DISEASE. 

Syphilis. — Owing to the great frequency of aortitis as a lesion 
of secondary syphilis, and since it so often involves the mouths of 
the coronary arteries, it is not surprising that blood-pressure 
variations and other cardiac symptoms should frequently be 
encountered. Two-thirds of the 228 cases studied by Grassmann 1 
showed cardiac disturbances — arhythmia, bradycardia, tachycardia, 
murmurs, dilatation, etc. He found that the blood-pressure, which 
is normal at first, soon gives place to hypotension and instability. 
As soon as aortic valvular leakage is established, the pressure 
changes take on the characteristic manifestations of this lesion 
(see page 235). In 80 per cent, of Grassmann's cases the pressure 
(von Basch sphygmomanometer) was below 80 mm. in the temporal 
artery. Some of these cases showed a further reduction of both 
pressure and hemoglobin on the institution of the mercurial 
treatment. 

Based upon a study of 50 hypertensive cases, 90 per cent, of which 
yielded either a positive Wassermann or luetin test, Stoll 2 has 
advanced the hypothesis that hereditary syphilis is one of the most 
common causes of hypertensive disease. He lays stress on the 
importance of performing a luetin test, especially if activated by a 
week's mixed treatment in hypertensive cases which have yielded 
a negative Wassermann test. He reports favorable results from 
specific treatment especially in patients with pressures below 200 
mm. Hg. without any apparent deleterious effects upon the kidney, 
even in cases in which the phthalein excretion was considerably 
reduced. The best results were obtained by administering mercury 
by inunction, and potassium iodid by mouth (see salvarsan, p. 341). 

Tuberculosis. — The fact that tuberculosis is generally associated 
with hypotension has long been recognized and is generally 

1 Klin. Untersuch. a. d. Kreislauforganen in Friihstadium d. Syphilis, Deut. Arch, 
f. klin. Med., 1901, lxix, 281. 

2 The Role of Syphilis in Hypertensive Cardiovascular Disease, Am. Jour. Med. 
Sci. 1915, cl, 178. 



214 BLOOD-PRESSURE IN CHRONIC INFECTIOUS DISEASE 

accepted. This applies to both the systolic and the diastolic press- 
ures. The hypotension is secondary to the tuberculous process. 
Thayer's figures are as follows: 









Peters' cases. 


Age. 


Normal. 


Tuberculosis. 


(Altitude 6000 ft.) 


10 to 20 


128.7 


100.33 


122 


20 to 30 


136.9 


101.0 


123 


30 to 40 


140.8 


94.0 


124 


40 to 50 


142.2 


105.5 


134 


50 to 60 


154.8 


105.0 


138 


60 + 


180.0 


114.0 





This table shows hypotension at all ages in tuberculous subjects. 
Peters explains his higher readings as due to the higher altitude 
(6000 feet) at Silver City, New Mexico, and construes the results 
as indicating the advantages of such an elevation in regard to 
treatment, but F. C. Smith 1 was unable to substantiate these 
findings. 

As in health, the pressures are lower in women than in men. 
Blood- pressure bears no definite relation to the stage of the disease, 
although it generally does to the degree of toxemia. Thus the 
pulse rate and the degree of temperature sometimes, although 
by no means always, bear an inverse relation to blood-pressure. 
Pressure tends to rise as the pulmonary condition improves. Arterial 
tension bears no definite relation to the hemoglobin content of 
the corpuscles nor to an antecedent gonorrhea, syphilis, alcoholism, 
or pneumonia. Stantion was able to corroborate in tuberculous 
subjects Thayer's statement that individuals who have had typhoid 
fever show disproportionately higher pressures later in life. A 
complicating nephritis may cause a rise of pressure, but rarely, 
if ever, to the degree attained in non-tuberculous cases. In the 
literature on the subject there is, however, much room for 
uncertainty, since the term "nephritis" as used in connection with 
tuberculosis may mean a tuberculous lesion engrafted on an old 
nephritis, amyloid disease, or a true tuberculous nephritis. In 
the latter condition, Reitter 2 found actual hypotonia as contrasted 
with other forms of pyelitis and pyelonephritis in which the pressure 
was at least normal if not distinctly increased. 

The vasomotor instability of tuberculosis is shown by the fact 
that at least a large proportion of the advanced cases show a fall 
of pressure and a considerable increase in pulse rate, on changing 
from the recumbent to the erect position. 

1 The Effect of Altitude on Blood-pressure, Jour. Am. Med. Assn., 1915. briv, 1812. 

2 Nierentuberkulose u. arterielle Hypotension, Zeit. f. klin. Med., 1907, lxii, 35S. 



TUBERCULOSIS 215 

Bouchard, Arloing, Rhodet, and Courmount believe that the 
toxin of the tubercle bacillus possesses distinct vasomotor influences. 
These results have been recently corroborated and much more 
satisfactorily demonstrated by Emerson. Man is apparently 
much less sensitive to this effect than animals, since a relatively 
larger and more concentrated dose is required to produce much 
fall of pressure. Whether this toxin is the sole cause of the hypo- 
tension is still undecided. For instance, it may result simply from 
tachycardia, for beyond a certain point systolic output falls with 
an increasing pulse rate, owing to insufficient diastolic inflow. 

"Fever will cause rapid heart action by its effect on the accelerans 
nerve endings in the heart. Diminished general pressure results 
in lower cerebral pressure, which of itself stimulates the cerebral 
origin of cardiac sympathetic nerves, especially when the low 
pressure is due to vasoparesis" (Krehl). 

Laryngeal and intestinal complications are often associated 
with low pressures. Arrested cases generally show a rise and 
relapsing cases a fall of tension. Ambulant patients yield higher 
readings than bed-fast cases. The cardiac hypertrophy seen in 
some cases in the early stages of tuberculosis is perhaps due to 
the effort of the heart to maintain an efficient circulation, despite 
the vascular relaxation. The late atrophy probably results from 
inanition and myocardial degeneration. 

There are three theories which have been used to explain the 
toxic hypotension of tuberculosis: 

1. That it is due directly and chiefly to the heart muscle, which 
is pathologically altered, either as the result of the toxins of the 
bacillus or as the result of malnutrition. 

2. That the bloodvessels are primarily the cause of the vaso- 
dilatation, which is the result of the tuberculous toxins. 

3. That the nervous control of both heart and bloodvessels is 
essentially influenced by the toxemia, both the vascular dilatation 
and the tachycardia being of nervous origin. 

Two practical facts present themselves: 

First. Is the study of pulse and blood-pressure of prognostic or 
therapeutic value, and is it of diagnostic value previous to the 
time when a diagnosis may be made from physical signs? 

Second. To what is the hypotension due, and to what extent 
can it be remedied by treatment? 

There are wide diversities of opinion on these subjects. Broadly 
speaking, the French writers maintain that hypotension is a valuable 



216 BLOOD-PRESSURE IN CHRONIC INFECTIOUS DISEASE 

early sign of tuberculosis, which may often be suspected on this 
account, even when latent; and further, that it is a valuable 
differential point in deciding between chlorosis, etc., and incipient 
tuberculosis, also in diagnosticating between tuberculous effusions 
in the pleura and in the peritoneum and non-tuberculous effusions. 
On the other hand, a large number of observers, of whom many 
are Germans, find that hypotension is inconstant, and when present 
only a late phenomenon. We agree essentially with the latter 
proposition, feeling that the stethoscope is a far better early 
diagnostic instrument than the sphygmomanometer, believing, 
however, that blood-pressure observations are capable of rendering 
useful data so far as the corroboration of diagnosis, the gauging 
of toxemia, the permitting of exercise, and the recognition of relapses 
are concerned. It is to be borne in mind, however, that there is a 
common type of constitutional hypotensive individual who has 
a low pressure without either active or latent tuberculous disease 
(see page 185). 

As to the actual causes of tuberculous hypotension, Haven 
Emerson, 1 who has published an excellent clinical and experimental 
study on the subject, arrives at the following conclusions: 

"The causes of low blood-pressure in tuberculosis are probably 
primarily a toxic action on the vasomotor centre in the medulla, 
allowing of a vasoparesis or stimulating an active vasodilatation, 
and, secondarily, progressive cardiac atrophy or degeneration. 
Toxic action on the vasomotor nerves or their motor terminals 
or on the nervous mechanism of the heart cannot be positively 
denied, although there is no proof of it at present. Toxic action 
of tubercle products has not been demonstrated on the muscle 
of the vessel wall or heart, although with regard to the latter, 
the degenerated heart muscle found in advanced cases may have 
an influence in causing hypotension. Rapid heart action is a usual 
and necessary sequel to low blood-pressure, and will, if extreme, 
aggravate the hypotension by the very act of its shortened diastole. 
It has been suggested, but not proved, that lack of vagus inhibition, 
owing to pressure by enlarged bronchial lymph nodes and the 
presence of sympathetic excitation from similar or reflex causes, 
such as pulmonary or gastric irritation, are responsible for the 
tachycardia and hypotension. 

"Hypotension or subnormal blood-pressure is universally found 

1 Blood-pressure in Tuberculosis, Arch. Int. Med., 1911, vii (bibliography). 



TUBERCULOSIS 217 

in advanced pulmonary tuberculosis, in which condition emacia- 
tion may be responsible for its causation. Hypotension is found in 
almost all cases of moderately advanced tuberculosis, or in early 
cases in which the toxemia is marked, except when arteriosclerosis, 
the so-called arthritic or gouty diathesis, chronic nephritis, or 
diabetes complicate the tuberculosis and bring about a normal 
pressure or a hypertension. Occasionally the period just preceding 
or during hemoptysis may show hypertension in a patient whose 
usual condition is that of hypotension. 

"Hypotension has been found by so many observers in early, 
doubtful, or suspected cases, with or before physical signs of the 
disease in the lungs, and is considered by competent clinicians 
so useful a differential sign between various conditions and 
tuberculosis, that it should be sought for as carefully as it is the 
custom at present to search for pulmonary signs. 

"Hypotension when found persistently in individuals or families 
or classes living under certain unhygienic conditions should put 
us on our guard against at least a predisposition to tuberculosis. 
Most unhygienic conditions, overwork, undernourishment, and 
insufficient air are of themselves causes of a diminished resistance, 
and it seems likely that a failure of normal cardiovascular response 
to exercise or change of position may be found to indicate this 
stage of susceptibility, especially to tuberculous infection. 

"The difficulty of proving subnormal pressure is so much greater 
than that of determining an increase of pulse rate, or of temperature, 
that some means such as the one I suggest in the tests I have 
made personally should be tried before considering a patient normal 
just because a single systolic reading shows a pressure within normal 
limits. 1 

"Hypotension, when it is present in tuberculosis, increases with 
an extension of the process. Recovery from hypotension accom- 
panies arrest or improvement. Return to a normal pressure is com- 
monly found in those who are cured. Continuation of hypotension 
seems never to accompany improvement. Prognosis can as safely 
be based on the alteration in the blood-pressure as on changes in 
the pulse or temperature. 

"The secondary anemia, with its diminished albumin, salts, and 
hemoglobin content, serves to add to the hypotension from purely 
physical causes in the blood-stream. 

1 The test consisted in pulse and pressure observations after change of posture. 



218 BLOOD-PRESSURE IN CHRONIC INFECTIOUS DISEASE 

"Diminished area of lung tissue, resulting in an increased carbon 
dioxid content of the blood, is suggested as a contributory cause of 
hypotension. 

"Displacement of the heart, which is so common a result of 
retracted lung tissue, or loss of expansion due to cavity formation 
or adhesive pleurisy, is spoken of as a cause of tachycardia accom- 
panying hypotension, and it certainly seems to be a contributory 
cause in some cases. 

"Marked vasomotor irritability is recognized as a frequent 
phenomenon in pulmonary tuberculosis, and is supposed to result 
in tachycardia and hypotension; but it is not easy to see exactly 
what is meant by this term unless it is a certain functional insta- 
bility for which we have no proof of any definite local cause. 

"Disease of the adrenal bodies is to be mentioned as a possible 
factor, only to be set aside for lack of any consistent pathological 
proof. 

"Primary cardiac atrophy, congenital or acquired, can no longer 
be considered as a factor in the presence of modern orthographic 
x-ray examinations, and in the absence of agreement among path- 
ologists. 

"The result of hypotension in tuberculosis or in any other condi- 
tion is insufficient capillary pressure, more or less venous stagnation 
of the essential organs of the body. 

"The treatment of tuberculosis in all its stages should take into 
consideration the need of assisting in every way the return to 
normal pressure, (1) by relieving the relaxed vessels of the load 
put on them during the vertical position or exercise, and (2) by 
assisting the heart by abundant nutrition, moderate exercise, and 
the stimulating effect on cardiac and vascular tone of cold fresh air, 
to meet the extra work put on it by the loss of vascular tone. Thus 
will the heart be able to maintain its normal bulk and strength, or 
even to gain from the atrophy or small size of the early disease 
to a normal size, so that brain, kidneys, lungs, and body at large 
may be properly nourished until the disease is arrested and the 
toxic products of the tubercle bacillus are no longer distributed 
from the site of the lesion." 

The question whether hemoptysis is associated with increased 
blood-pressure has received both affirmation and denial. Nor is 
this surprising when we remember that the pressures in the pulmo- 
nary and in the systemic circulation vary independently of each 
other. A progressive diminution of the pulse pressure indicates 



TUBERCULOSIS 219 

continued hemorrhage. At the time of actual hemorrhage the 
excitement incidental thereto tends to increase blood-pressure. 
There appears to be no ground to support the contention that 
hemorrhage occurs most frequently in cases with a high systolic 
pressure. The establishment of an artificial pneumothorax is like- 
wise without any constant influence on arterial tension. 1 In one 
of Smith's cases there w r as a marked unilateral pressure difference 
associated with incomplete collapse of the lung clue to pleural 
adhesions. 

Blood-pressure estimations have been used as a gauge whereby 
to control exercise in the tuberculous. Peters 2 decreases the amount 
of exercise if the patient shows a drop of 6 mm. or more after one 
hour's rest, or if exertion is immediately followed by a marked 
fall (10 to 20 mm.) of pressure. 

The Treatment of Pulmonary Hemorrhage. — Both clinically and 
experimentally, hemorrhages from the pulmonary vessels tend, to 
cease spontaneously, owing to the low blood-pressure in the pul- 
monary circuit and to the reticulated nature of the lung paren- 
chyma. In animals it is difficult to produce a fatal result, even 
when the main branch of a lobe is cut. The protective mechanism 
in man seems to be less efficient. The great discrepancy which 
exists regarding methods of treatment is due to the fact that a 
distinction is not made between the early and late stages of hemor- 
rhage in which the physiologic principles in therapeusis are radi- 
cally different. Digitalis, atropin, the nitrites, aconite, chloral, 
chloroform, ergot, adrenalin, pituitrin, and other substances, have 
been recommended. 

We have to consider (1) the effect of the drug on the pulmonary 
and (2) on the general arterial blood-pressures; (3) its effect on the 
small pulmonary arterioles; (4) its effect on heart rate and systolic 
output; (5) its effect on the respiratory centre. Generally speaking, 
a reduction of pulmonary pressure should reduce hemorrhage, but 
if this is done at the cost of an increased systolic output it will, of 
course, not do so. Constriction of the small pulmonary vessels tends 
to increase pressure in the pulmonary arteries and thus to increase 
bleeding. It is evident, therefore, that the ability to constrict the 
pulmonary vessels is not a criterion of its hemostatic value. The 
maintenance of a normal mean pressure in the pulmonary circuit 

1 Smith, F. C, The Effect of Altitude on Blood-pressure, Jour. Am. Med. Assn., 
1915, lxiv, 1S12. 

2 Blood-pressure Control of Exercise in Tuberculosis, Colorado Medicine, 1915, xii. 



220 BLOOD-PRESSURE IN CHRONIC INFECTIOUS DISEASE 

is a function which Nature tends to accomplish in spite of inter- 
ference, just as it does in the case of cerebral anemia. Because 
we lower the systemic pressure, it of course does not follow that 
we lower the pulmonary pressure. Furthermore, in the late stages 
of bleeding cerebral anemia is prevented by splanchnic vasocon- 
striction. To thwart this result might produce death, which is 
certainly a strong argument against the use of the nitrites. What 
we are attempting to accomplish, is to reduce pressure in or reflux 
from the pulmonary vessels without embarrassing the respiratory 
or vasomotor centres or the heart in their efforts to maintain the 
circulation. 

The physiologic effect of certain drags upon the pulmonary and 
systemic circulations. 

Digitalis (without alcohol) produces a rise of pulmonary pressure, 
slight at first, but increasing as its action becomes more pronounced. 
It therefore increases hemorrhage by augmenting the systolic output 
of the right ventricle and constricting the pulmonary vessels. 

Ergot primarily decreases pulmonary arterial pressure by depress- 
ing the heart. It is followed, especially in normal animals, by an 
increase due to a secondary augmentation of the beat. Pressure 
in hemorrhage in the pulmonary veins is permanently increased 
at the constriction of the small vessels. The action of the drug 
wanes as the loss of blood continues. 

Pituitrin. — This drug has been highly recommended by Wiggers, 
since it elevates the systemic arterial pressure through vasocon- 
striction in spite of weakening of the left heart. The decrease in 
amplitude of contraction of the right ventricle causes a fall of 
pulmonary pressure, which neither the weak constricting influence 
of the blood on these vessels nor the backing up of the blood from 
the left heart counteracts. It does not affect the respiratory centre. 
These results occur both in normal and in bleeding animals. 

Chloroform produces a fall of pressure in the pulmonary circuit 
due to depression of the heart and aided by diminished respiration. 
During dyspnea in hemorrhage small doses lessen the respiratory 
movements and so decrease pulmonary pressure and hemorrhage, 
while large doses act similarly through cardiac depression. 

The Nitrites. — In normal-breathing animals a general increase 
in pulmonary pressure is noted, due to increased rate and systolic 
output of the heart. In animals breathing rapidly from hemorrhage, 
nitrites increase both pressure and hemorrhage from pulmonary 
arteries and veins. In the stage in which the nitrites reduce the 



TUBERCULOSIS 221 

amplitude of respiration a lowering of the pulmonary pressure and 
a reduction of hemorrhage occurs. 

It is essential in the treatment of hemoptysis, as was shown 
by Wiggers 1 (from whose articles many of the foregoing data 
were taken), to differentiate between the early and the late stages 
of the hemorrhagic process. 

Effect of Various Agents on Systemic Pressure, Respiration, Pulmonary 

Arterial Pressure and Hemorrhage, and Pulmonary Venous 

Pressure and Hemorrhage. (Wiggers.) 

Pulmonary Pulmonary 
arterial venous 

Systemic pressure and pressure and 

Drugs. pressure. Respiration. hemorrhage. hemorrhage. 

Digitalis: 

Normal + + (-) + 

Hemorrhage + + + 

Strophanthin : 

Normal \ . „ , . 

Hemorrhage/ 
Ergo toxin: 

Normal + — h — 

Hemorrhage .... — 

Pituitary: 

Normal + - or ( +) - - 

Hemorrhage . . . . + — — — 

Chlorof orm : 

Normal \ 

Hemorrhage/ 
Nitrites: 

Normal - + + 

Hemorrhages early ..— + (— )+ (— ) + 

Late — — — — 

Summary. — In the early stage of hemorrhage, in a practically 
normal subject with only occasional coughing, pulmonary pressure 
should be reduced by means of cardiac depressants, chloroform, or 
pituitary extract. The nitrites are contra-indicated. In the late 
stages, with tachycardia and tachypnea, the heart and bloodvessels 
no longer react in a typical manner to certain drugs. Cerebral 
anemia manifests itself. The blood-supply of the brain must 
be maintained. According to Wiggers, the only drug which can 
elevate the systemic pressure and simultaneously lower the pul- 
monary pressure is pituitary extract. 

All clinical and most experimental evidence indicates that 
morphin is the most valuable drug we possess in the treatment of 
hemoptysis. Fear and excitement are among the most potent causes 

1 A Physiological Investigation of the Treatment of Hemoptysis, Arch. Int. Med. 
July 15, 1911; Studies in Inaccessible Internal Hemorrhages, Ibid., March, 1909. 



222 BLOOD-PRESSURE IN CHRONIC INFECTIOUS DISEASE . 

of increased arterial tension in general, and probably in the pul- 
monary circulation, and under these conditions nervous sedatives 
are the most rational form of therapy. 

Recent experiments, however, show that morphin may be harmful 
when death is threatened by a hemorrhagic fall of pressure. There 
are two factors to be considered: (1) Augmented breathing acts 
favorably from a mechanical point of view in maintaining blood- 
pressure. (2) Excessive breathing may produce acapnia and 
cause a fall of blood-pressure. Wiggers 1 maintains that the former 
condition outweighs the latter in importance, and that morphin 
must be employed with caution. This statement, of course, applies 
only in the case of large hemorrhages in which death is to be feared, 
and the evidence furnished cannot be used to negative the well- 
attested clinical results which have shown the good effects of 
morphin. 

Pleural Effusions. — The existence of pleural and peritoneal effu- 
sions, especially if large, tend to increase blood-pressure, and their 
removal is attended with a fall of arterial tension. The pressure, 
therefore, of such serous effusions may increase a pressure already 
high as the result of nephritis, and a fall of pressure following 
aspiration may not indicate any improvement in the basic condition 
from which the patient suffers. On the other hand, a cardiac 
hydrothorax may cause a pressure sufficiently high to make one 
suspect a coincident nephritis when no such complication exists. 

The emotional disturbance entailed by a prospective operation as 
well as the actual pa.in of puncture produce a temporary elevation 
of blood-pressure. Aspiration of a pleural exudate is attended by 
a gradual fall of blood-pressure which occurs pari passu with the 
withdrawal of fluid. According to Capps, 2 a fall of 20 mm. is 
usual. The systolic pressure is chiefly affected. This fall of pressure 
is probably not merely the result of the mechanical pressure effects, 
but is in part due to vasodilator and cardio-inhibitory reflexes. 

After withdrawal there is a gradual rise of pressure, but the initial 
limit may not be reached for some time. The rate of withdrawal 
is no less important than the amount of fluid removed in its effect 
on the immediate fall of pressure. The more long standing, the 
effusion the greater the fall of pressure, probably due to imperfect 

1 C. J. Wiggers, K. C. Eberly, and H. L. Wenner, The Pressor Influence of Aug- 
mented Breathing, Jour. Exp. Med., 1912, p. 174. 

2 Observations on the Effect on the Blood-pressure of Withdrawal of Fluid from 
the Thorax and Abdomen, Jour. Amer. Med. Assn., January 5, 1907, xlviii. 



PNEUMO THOR. 1 X 223 

pulmonary expansion. Marked reactions and a slow recovery are 
seen in arteriosclerotic cases. 

By observing the blood-pressure during thoracentesis, untoward 
effects such as weakness, vertigo or collapse, symptoms which 
often occur suddenly and without warning, may be anticipated 
and obviated. (See Aspiration of the Pleura, page 38G). 

Pneumothorax. — Pneumothorax and penetrating wounds of the 
chest, in addition to well-known symptoms, are often associated 
with bradycardia and a rise of blood-pressure (presenting some- 
times an analogy to cerebral injuries), from which signs too opti- 
mistic conclusions may easily be drawn. 

Experimental Data. — The reports to be found in literature on 
blood-pressure in artificial pneumothorax are very divergent. 
Kakowski 1 and others report a rise in open pneumothoraces, 
other investigators no change, and still others a fall of blood- 
pressure. 

According to Walther experimental pneumothorax in the normally 
breathing rabbit is associated with a slowing and an increase in 
the volume of the pulse. Elimination of vagus control does not 
check the rise of pressure which is apparently due to C0 2 stimulation 
of the vasomotor centre. The change in the pulse rate, on the 
other hand, is believed to result from vagus stimulation. The 
difference in response between an open and a closed pneumothorax, 
which is only one of degree, has been explained as due to the fact 
that in the latter, in addition to stimuli which result from pleural 
irritation, those arising in the bronchial mucous membrane (since 
respiratory excursions are still present) are superadded. The 
irritation of the pleura is conducted by the sensory fibers of the 
vagus to the nucleus and produces increased vagus tone. 2 

Clinical Data. — Spontaneous pneumothorax may come on sud- 
denly with acute pain and shock, especially if the onset occurs 
during exercise in apparently healthy individuals. Frequently, 
however, pneumothorax occurs insidiously 3 during the course of 
tuberculosis. In the former instance a primary fall of blood- 
pressure is succeeded by a rise to above the normal, which is in 
part at least the result of anxiety, pain, and asphyxia. In the latter 

1 Zur Frage d. Kunstliehcn Pneumothorax, Pfliigcr's Arch., 1910, exxxiv, 31. 

2 Walther, H. E., Zur Kentniss der Puis u. Blutdruckveranderungen beim Pneu- 
mothorax, Deut. Zeitsch. f. Chir., 1912, cxix, 253. 

3 Among 500 cases of pneumothorax the onset was sudden in 77 and insidious in 
23 per cent, of the cases. The latter class was evidently underestimated. Pepper, 
O. H. P., Amer. Jour. Med. Sci., October, 1911. 



224 BLOOD-PRESSURE IN CHRONIC INFECTIOUS DISEASE 

instance blood-pressure changes are neither constant nor marked, 
especially if only a partial pneumothorax is present. 

There is considerable reason to believe that the occurrence of 
pneumothorax in the course of tuberculosis may have beneficial 
effects. Certainly the artificial production of this condition is 
often attended with marked symptomatic improvement. Just 
to what extent this is due to changes in the pulmonary circulation 
is as yet uncertain. "It is disputable as to whether the contracted 
lung contains more or less venous blood. In fact, there is experi- 
mental evidence that the pulmonary circulation adapts itself 
promptly to the change and is therefore not particularly dis- 
turbed." 1 

Symptoms of shock and occasionally sudden death have followed 
the therapeutic establishment of pneumothorax. Such events are 
generally due to a pleural reflex which consists of afferent medullary 
impulses by way of the vagus nerve from its terminal filaments, 
which have been rendered unduly susceptible to stimuli as a result 
of compression or inflammation. Death is apparently due to vaso- 
constriction of the cardiac or cerebral vessels. Artificial pneumo- 
thorax should never be employed in the presence of severe cardiac 
complications. 2 

1 Robinson, S., and Floyd, C, Artificial Pneumothorax as a Treatment of Pul- 
monary Tuberculosis, Arch. Int. Med., 1912, ix, 452. 

2 Sachs, T. B., Artificial Pneumothorax in the Treatment of Pulmonary Tuber- 
culosis, Jour. Amer. Med. Assn., 1915, lxv, 1861. 






CHAPTER IX. 

EXOGENOUS INTOXICATIONS. 

Lead Poisoning. — The most important exogenous intoxication, 
so far as blood-pressure is concerned, is lead poisoning. Hyper- 
tension is produced directly as the result of plumbism and indirectly 
as a result of gout, nephritis, or arteriosclerosis, 1 with each of 
which conditions plumbism is closely allied. The onset of both 
lead colic and encephalopathy is associated with marked exacerba- 
tions of pressure even in the absence of nephritis or gross vascular 
lesions. This increase in pressure is believed to be the result of 
vascular spasm, since it disappears after the paroxysm. The arterial 
constriction is evident on examination of the retinal vessels; and 
Pal has reported a case of lead amaurosis which appeared with 
the onset and disappeared with the abeyance of hypertension. 
The systolic pressure is chiefly affected, and large as well as sudden 
variations of pressure are often encountered. Extended observa- 
tions have shown that 80 per cent, of all lead-workers exhibit high 
arterial pressure over years of time even when free from symptoms 
of poisoning, a fact which might be expected if the contention of 
Schmidt, 2 be correct that no real elimination of lead ever occurs, 
once it has entered the body, but merely a transference of it to 
different tissues. Most but not all cases of colic show an exacerba- 
tion of tension coincidently with the colic. The actual pressure 
does not generally exceed 200 mm. Hg. except in cases of enceph- 
alopathy. It seems eminently likely that the pain markedly 
augments the pressure. But that pain is not the essential cause 
is shown by the fact that lowering of pressure relieves it (Riegel, 
Frank, Bardenhauer), while relief of the pain with morphia does 
not lower the tension (Riegel, Borgen), nor does pressure always 
fall with a spontaneous relief from colic. It has, on the other 
hand, been maintained that the pressure is compensatory, and 

1 The vascular changes differ from those of ordinary arteriosclerosis. The vessels 
do not collapse and exhibit a normal intima with marked hypertrophy of the media. 
Cardiac hypertrophy is not constant. 

2 Untersuchungen bei experimenteller Bleivergiftung, Deut. Arch. f. klin. Med., 
1909, xcvi, 587. 

15 



226 EXOGENOUS INTOXICATIONS 

when sufficiently high prevents the colic. The latter view does 
not commend itself. The hypertension has also been attributed 
to the effect of lead on the central nervous system. It has also 
been suggested that the hypertension is due to increased adrenal 
secretion. Heubel 1 maintains that the rise of pressure is purely 
secondary nephritis, etc.; while Broadbent attributes it to the 
chemical formation of lead albuminates, which, being with difficulty 
broken down, complicate metabolic changes and render the elim- 
ination of metabolites difficult. Menetrier and others believe that 
arterial hypertension is a primary and initial toxic phenomenon. 

Lead colic is generally regarded as due to involvement of the 
solar plexus. Thus, Laignel-Lavastine speaks of the pain, con- 
stipation, and hypertension as symptoms of "solar stimulation." 
Lesions of the ganglia of the plexus have been demonstrated post- 
mortem (Tanquerel, Kussmaul, Maier) and experimentally (Mosse) . 

Experimental Data. — The intravenous injection of lead salts 
produces arterial hypertension. Of course, it does not follow 
because acute intoxication produces this effect that therefore 
chronic poisoning will have similar results. The chief physiological 
action of lead is exerted on striated muscle, in which it produces a 
diminished functionation (Nothnagel and Rossbach). This would 
lead to vasomotor relaxation, and unless it were counterbalanced 
by compensatory vasoconstriction, to a fall of pressure. According 
to Jores, 2 such a relaxation occurs in the smaller arteries of rabbits 
poisoned with lead. 

Clinical Data. — Hypertension has long been observed clinically 
(Riegel and Frank). The presence of hypertension, especially if 
nephritis can be eliminated, should certainly suggest the possibility 
of plumbism even if the gingival blue line or basophilic degeneration 
of the erythrocytes cannot be demonstrated. Arterial stasis alone 
will not increase pressure, and since there is a marked hypertension 
during attacks of colic, we must assume a vasoconstriction, either 
as the result of a toxic effect or owing to some compensatory 
antagonistic physiologic action (central vasoconstriction?). 

Furthermore, as shown by Hasebroek, the sphygmograph of a 
lead pulse is more like that of a normal pulse than that of an arterial 
hypertension. He uses this and some of the foregoing arguments 
to establish the existence of an active arterial diastole, and believes 

1 Path. u. Sympt. der chr. Bleivergiftung, Berlin. 

2 Ueber die path. Anat. d. chronischen Bleivergiftung des Kaninchens, Miinch. 
med. Woch., 1902, p. 713. 



ENCEPHA LOP A Til Y 227 

that plumbic hypertension results not from vascular spasm but from 
an "increased activity of the pressor components of physiologic 
vascular functionation." Stewart in his studies on blood-flow found 
in lead poisoning without paralysis a conspicuous tendency to reflex 
vasoconstriction. 

Well-marked bradycardia is quite common. In 1179 cases 
Tanquerel found the pulse rate between 20 and 60 in 078, between 
65 and 70 in 376, and between 80 and 100 in 125 cases. Such cases 
are a true bradycardia due, it appears, to a toxic effect upon the 
vagus nerve or its terminations. The bradycardia and the arterial 
hypertension are independent phenomena. 1 

Encephalopathy. — In this condition very high pressures are often 
encountered. Menetrier 2 attributes the symptoms to the high 
pressure. 

In a man, aged twenty-one years, during one of many attacks 
of colic, a pressure of 260 mm. was found which soon reached 300 
mm. and was then associated with marked cerebral symptoms. 
At autopsy the kidneys were normal, as had been the urinary 
findings during life. The brain showed marked signs of pressure, 
edema, distended membranes, flattened convolutions, etc. 

It appears, therefore, that plumbism may be accompanied by 
numerous clinical manifestations which strongly suggest vascular 
spasm as the basis of their production. Thus the abdominal colic, 
anginoid attacks, encephalopathy, including amaurosis, hemianopia, 
aphasia, deafness, etc., have been attributed to local vascular 
contraction. 

Although generally associated there is no absolute parallelism 
between pain and vascular spasm; either may exist without the 
other. It is not yet proved that lead colic is due (1) to spasm of 
intestines or to (2) spasm of mesenteric arteries. It is apparently 
associated with a general vascular spasm in which, of course, the 
splanchnics have a part. Such a general contraction may begin 
suddenly or gradually, hence it is often difficult to say what the 
individual's normal is. The fact that pain is absent is no proof that 
the vessels are not contracted. Hypotension (55 to 75 mm. Hg.) 
may follow colicky attacks. Relief from constipation often goes 
hand-in-hand with the disappearance of pain and with a fall of 
pressure (Riegel). 

With so many divergent theories and such unequivocal experi- 

1 Lion and Marcorelles, Presse Med., 1913, No. 12, p. 109. 

2 Soc. med. des Hopitaux, February 12, 1904. 



228 EXOGENOUS INTOXICATIONS 

mental and clinical findings, we must therefore conclude by saying 
that although in lead poisoning hypertension is constant, and exac- 
erbations of tension frequent, we are still unable to make positive 
statement as to the exact mechanism by virtue of which these 
vascular phenomena are produced, or whether they are primary 
or secondary manifestations. Persistent marked hypertension is 
of bad augury in plumbism. Borgen has observed the following 
phenomena in cases of lead colic: (1) period of rising pressure, 
of variable duration; (2) period of high pressure, one to four days; 
either of the above may be associated with colic; (3) period of 
decrease, two to four days, with disappearance of. symptoms; (4) 
period of subnormal pressure (95 mm.). . 

Therapeutics. — If the conception of the pathologic process as a 
local (or general) vascular spasm is correct then purgation with 
salines and belladonna is a rational procedure. The administration 
of morphin is purely palliative. Pal endorses the custom sanctioned 
— administration of the iodides in large doses — saying that symp- 
toms of lead colic cease as soon as those of iodism appear. Some 
researches have thrown doubt upon the efficacy of the iodides, 
at least so far as elimination is concerned, and have suggested 
the employment of bile salts. The administration of the nitrites 
sometimes relieves pain. 

Phosphorus. — Acute phosphorus poisoning so far as the cir- 
culation is concerned, produces a degeneration of the heart muscle, 
and while this is doubtless a contributing factor in the cause of 
death, it appears from Pal's investigations that the primary cause 
lies in a fall of blood-pressure due to loss of vasomotor tone. 

Chlorin Gas — The inhalation of chlorin gas which has been used, 
in trench warfare causes a marked fall in blood-pressure, a slowing 
and irregularity of respiration and pulmonary symptoms which are 
apparently due to obstruction of the pulmonary circulation rather 
than to spasm occlusion of the bronchioles. 1 

Arsenic. — Acute arsenical poisoning causes a fall of blood-pressure 
due to depression of the heart and the vasomotor centre. 

Tobacco. — There has been much discussion as to whether the 
constitutional effects which follow the use of tobacco are due to 
nicotin or to the other substances. The evidence at hand indicates 
that nicotin is by far the most important, if not the sole factor, 

1 Sch&fer, E., On the Immediate Effects of the Inhalation of Chlorin Gas, British 
Mod. Jour., August 14, 1915, p. 245. 



TOBACCO 229 

but other substances, such as carbon monoxid, hydrocyanic acid, 
furfural and other aldehyds, have also to be reckoned with. 

Lehman has shown that the slower the rate of smoking the smaller 
the amount of hydrocyanic acid formed. This substance, however, 
seems to be present in too small amounts to account for physiologic 
symptoms. The ordinary cheap cigarettes (Virginia tobacco) 
contain only a negligible quantity of nicotin. They do, however, 
contain a large quantity of furfural to which the harmful effects 
may be due, yet this substance is practically absent from Turkish 
cigarettes. 1 

Experimental Data. — With moderate quantities of nicotin the 
pulse rate is slowed ; the heart may stop for a few seconds in diastole, 
then gradually assume an accelerated rhythm. The slowing is due 
to stimulation of the vagus ganglia. " It is not affected by section 
of the cervical pneumogastric, as the path from the ganglia to the 
cardiac ganglia is still intact, but, on the other hand, it is prevented 
by atropin, which acts on the extreme terminations of the inhibitory 
fibers, and therefore blocks the passages of impulses from the ganglia 
to the muscle." 

Blood-pressure is increased owing partly to stimulation of the 
vasoconstrictor centre in the medulla, but chiefly to peripheral 
influences, for it occurs even after extirpation of the spinal cord. 
"The vasoconstrictor nerves pass through ganglia on their way 
to the vessels, and the rise of blood-pressure seems to be mainly 
caused by a stimulation of these ganglia." (Cushny.) Hemorrhage 
causes a marked increase in the vasomotor reaction to nicotin. 2 

The fact that on analysis a certain variety of tobacco is shown 
to contain a greater or a smaller quantity of nicotin by no means 
proves that when smoked it will yield an equivalent amount. In 
fact the very opposite result may be obtained. The nicotin content 
of the smoke depends largely on the completeness and quickness 
of combustion. Ordinarily, half of the nicotin is destroyed by 
combustion. Of the remainder variable quantities reach the mouth, 
being carried there by the hot smoke, which, in passing through the 
condensation area, volatilizes certain substances in the tobacco. 
Hence, the larger the condensation area (long, thick cigars) the 
greater the amount of nicotin, etc., which comes through. 

The smoking of tobacco in the form of cigarettes is, for an equal 
amount of this substance consumed, less harmful than when used 

1 See editorial, Jour. Amer. Med. Assn., 1912, lix, 1798. 

2 Hoskins, Rowley and Rosser, Arch. Int. Med., 1915, xvi, 45G. 



230 EXOGENOUS INTOXICATIONS 

in the form of cigars or a pipe, assuming of course that inhalation 
is practised in each instance, because of the more complete combus- 
tion which ensues. Long cigars are relatively more injurious than 
short ones because they furnish a large condensation area in which 
the unconsumed nicotin accumulates. The last third of the cigar 
is, therefore, more toxic than the first two-thirds. For the same 
reason a cigar which has ceased to burn should not be relighted. 1 
The habit of holding an extinguished cigar between the lips should 
not be practised. Long-stemmed pipes are better than short ones. 

Tobacco and Arteriosclerosis. — The importance of tobacco as an 
etiologic factor in arteriosclerosis has been much discussed and the 
question still remains unsettled. The tobacco habit is usually 
coupled with the use of alcohol and frequently with faulty methods 
of living. It has yet to be shown that the career of smokers is 
shorter than that of non-smokers. It is admitted that tobacco is 
. a cardiovascular poison which is at first an excitant to the neuro- 
muscular apparatus, later a motor nerve depressant, and finally a 
paralyzant of the cardiac nerves. But whether it produces arterio- 
sclerosis, either by its direct toxic action on the vessels or indirectly 
by its effect on blood-pressure, is a very different question. Lee 
apparently succeeded in producing definite vascular lesions in 
rabbits which were made to inhale tobacco smoke over prolonged 
periods of time. Tobacco does no one any good, but it harms some 
less than others. The moderate smoking of tobacco in one who 
is accustomed to its use has but little effect on blood-pressure, 
and from a practical stand-point as a noxious factor is often 
negligible. 

Clinical Data. — There are of course individual differences, but 
generally tobacco tends to raise both the pulse rate and the blood- 
pressure, the former being in part the cause of the latter. These 
effects often appear after the first inhalation of smoke, and may 
be accompanied by a sensation of nervousness and sometimes 
precordial fulness or palpitation. The secretion of the adrenals is 
controlled by the sympathetic nerve, which is at first stimulated 
and later depressed by the administration of nicotin. 2 

The elevation of blood-pressure ranges between 3 and 25 mm., 
the systolic pressure being chiefly affected, indicating that the heart 

1 Lee, W. E., The Action of Tobacco Smoke, with Special Reference to Arterial 
Pressure and Degeneration, Quart. Jour. Physiol., 190S, p. 335. 

2 Cannon, Aub, and Binger, A Note on the Effect of Nicotin Injection on Adrenal 
Secretion, Jour. Phar. and Exp. Therap., 1912, iii, 379. 



DELIRIUM TREMENS 231 

is more affected than the bloodvessels. Pressure generally falls 
to or slightly below the original level within twenty minutes. Hesse 1 
found these results more marked in smokers than in non-smokers. 
The greatest rise in the pulse rate was twenty-five beats per minute. 
A return to the normal occurs in from twenty to forty minutes. 
Excessive quantities of nicotin cause a fall of pressure from depres- 
sion of the vasomotor centre and may in this way actually cause 
collapse. Strong tobacco causes more marked effects than the 
weaker varieties and in strongly reacting individuals the pressure 
may remain high for two hours. 2 Acute tobacco poisoning causes 
a fall of blood-pressure, associated with nausea, vomiting, vertigo, 
and sudation. 

Tobacco, then, should be forbidden, or its consumption limited 
when (1) we wish to spare the heart — cardiac, renal, pulmonary 
disease, etc.; (2) in arterial hypertension; (3) in arteriosclerosis. 

Chronic Alcoholism. — Chronic alcoholism is associated with 
variable blood-pressure, depending upon the extent to which renal 
and cardiovascular changes have occurred. But alcoholics in whom 
these organs are sound, show, when abstinence has been enforced, 
a marked rise of the systolic pressure followed after a few days by 
a gradual fall. The diastolic pressure is constantly high. Raff 3 
finds these results so constantly as to be of diagnostic value in 
differentiating between alcoholism and functional neuroses. 

Delirium Tremens. — In the asthenic type of case the systolic 
pressure is uniformly low and the pulse pressure small. A reestab- 
lishment of normal relations goes hand-in-hand with the subsidence 
of delirium. This would indicate that the height of blood-pressure, 
through its effect on the cerebral circulation, bears a causal relation 
to the delirium, a statement which is further borne out by the fact 
that if more normal values can be temporarily established by what- 
ever means, symptomatic improvement occurs (Pettey). 4 The 
treatment of delirium tremens by means of lumbar puncture has 
been attended by excellent results. It appears that the delirium 
is in part due to increased cerebrospinal pressure, and in part to 
toxicity of the spinal fluid. As pointed out elsewhere there is no 



1 Deut. Arch. f. klin. Med., March 15, 1907. 

2 John, M., Ueber d. Beeinflussung des systolischen u. diastolischen Blutdrucks 
durch Tabakrauchen, Zeitsch. f. exp. Path. u. Therap., 1913, xiv, 352. 

3 Blutdruckmessungen bei Alkoholikern u. funktionellen neurosen unter Ausschluss 
von Kreislaufstorungen, Deut. Arch. f. klin. Med., 1913, cxii, 209. 

4 The Narcotic Drug Diseases and ARied Ailments, Philadelphia, 1913, p. 99. 



232 EXOGENOUS INTOXICATIONS 

constant relationship between arterial and cerebrospinal pressure. 
(See Meningitis, and Lumbar Puncture.) 

Morphinism. — According to Pettey, morphin habitues generally 
show a high pressure due largely, it seems, to portal congestion, 
since evacuation of the bowels often causes a fall of from 30 to 60 
mm. Hg. "This reduction of arterial tension by the preparatory 
treatment, now universally verified, is an essential factor in prevent- 
ing collapse and other dangerous complications during the with- 
drawal period." 

Patients admitted with a blood-pressure of 180 to 200 mm. were 
usually found to have a blood-pressure of 140 to 150 after the system 
had been cleansed of toxic matter and the drug withdrawn. The 
lowered record is maintained throughout - convalescence, showing 
that it was the individual's normal pressure. 

The experience of the Avriter with this class of patients has been 
limited, but he nevertheless feels that the preceding statements 
must be accepted with reserve. Certainly, patients with the opium 
habit as seen in our hospitals are generally admitted in a condition 
of semicollapse, due to starvation, intoxication, and cachexia, with 
blood-pressure distinctly below the normal. 

Yalenti 1 found that if morphin were withdrawn from dogs which 
had become accustomed to its use, marked circulatory disturbances 
such as arterial hypotension, arhythmia and tachycardia occurred. 
These symptoms abated if the use of the drug was renewed. 
Furthermore, the serum of dogs suddenly deprived of morphin 
caused similar symptoms when injected into other dogs, whereas 
the serum of unmorphinized dogs has no such effect. It seems 
evident, therefore, that during the withdrawal stage, circulation 
stimulation may be necessary. 

1 Experimentelle Untorsuohungen ii. d. chronischen Morphinismus, etc., Arch. f. 
exper. Path. u. Pharmakol., 1914, lxxv, 437. 



CHAPTER X. 
BLOOD-PRESSURE IN CARDIAC DISEASE, Etc. 

Mechanical Hypotension. — 'When the total volume of blood is 
diminished from whatever cause (hemorrhage, diarrhea, sweating, 
polyuria) a fall of blood-pressure may result. For a time, of course, 
this may be counterbalanced by arterial constriction. Such a 
hypotension is seen typically in postpartum hemorrhages. Whether 
the hypotension seen in severe anemias, often with a diminished 
viscosity, has a similar genesis cannot be positively asserted. 

Factors which hinder the flow of blood to or from the right 
heart (a fall of venous pressure, adhesive or effusive pericarditis, 
obstruction in the pulmonary circuit, portal or caval obstruction, 
etc.) produce arterial hypotension. The removal of serous effusions 
from the peritoneum or pleura tends to produce a similar effect, 
as do also cardiac and valvular lesions in the stage of broken 
compensation. 

Functional Hypotension. — This form of hypotension occurs when 
vascular tone, especially in the splanchnic vessels, is below the 
normal or when a local vasodilation is insufficiently compensated by 
local constriction elsewhere. It is seen chiefly in fevers (toxemia), 
in constitutional low arterial tension, and in medical or surgical 
shock. 

Terminal Hypotension. — Terminal hypotension may result either 
from mechanical or functional causes. By this term we mean the 
ultimate fall of pressure which occurs as a result of cardiovascular 
failure. It is seen in the agonal and preagonal periods. It is com- 
mon as the terminal stage of hypertension, in which the pressure 
may be only relatively, not actually, below the normal. Occasion- 
ally life may be maintained for several hours or even days with a 
maximum pressure of 60 mm. Hg.; indeed, figures as low as 45 mm. 
(associated with unconsciousness and a subnormal temperature) 
have been reported by Xeu. 

Diseases of the Heart. — Despite the great abnormalities of the 
circulation, which are manifest during the course of valvular and 



234 BLOOD-PRESSURE IN CARDIAC DISEASE 

myocardial disease, pressure observations often show relatively 
insignificant changes. Increased blood-pressure is essentially a 
vascular and myocardial, not a valvular phenomenon. Excluding 
the conspicuous findings of aortic insufficiency and cardiorenal 
hypertension, sphygmomanometric readings often are of discourag- 
ingly little clinical value, although a normal systolic, associated 
with a high diastolic, pressure is very suggestive of cardiovascular 
disease. This is due to the fact that although the general systemic 
pressure may be normal, the rapidity of blood-flow, the mass move- 
ment of the blood, and especially the normal pressure relations 
between the arteries, arterioles, capillaries and veins have been 
either locally or generally disturbed. Regarding these conditions 
ordinary sphygmomanometric observations teach us but little by 
inference and nothing directly. 

Frequently in valvular disease one finds diminished pressure, 
100 to 110 mm., but such a hypotension is more often attributable 
to coincident conditions, such as fever, etc., than to a direct cardiac 
effect. In acute rheumatic endocarditis the pressure is not different 
from that in old valvular lesions. Rarely blood-pressure and tem- 
perature rise and fall together. Only exceptionally does the pressure 
in afebrile cases fall below 90. Not infrequently pressure values 
remain the same in broken compensation and during subsequent 
improvement. Digitalis produces practically no rise of pressure 
in valvular cases. (D. Gerhardt.) 

We may have a stasis of blood due to increased resistance in 
the peripheral arteries without elevation of either the systolic or 
the diastolic pressure. The condition which Sahli has described 
as high pressure stasis ("hochdruckstauung") occurs when the 
arterioles are tonically contracted or sclerotic so that outflow is 
prevented. Under such circumstances even an insufficient heart 
may, by forcing gradually more blood into the arterial reservoir, 
increase the pressure. This is further abetted by the accumulation 
of C0 2 in the blood, which, by stimulating the vasomotor centre, 
leads to still further arterial contraction. 

In these cases a plethoric, cyanotic face is often associated with 
edema and other evidences of cardiac failure, together with high 
arterial tension, which falls when circulatory improvement occurs. 
A fall of pressure is of serious import chiefly when associated with 
a rise of venous pressure, the latter being manifested by hepatic and 
pulmonary congestion. Vascular reflexes are sometimes abolished 



AORTIC LESIONS 235 

in advanced cardiac disease. Cases of cardiac decompensation 
often show a fall of pressure coincident with subjective and objective 
improvement. This is attributable to better renal elimination, 
to diminution of the C0 2 content of the blood, and to a diminution 
of hydremic plethora (see page 268). 

Aortic Lesions. — Experimental Data. — The establishment of ex- 
perimental aortic insufficiency in animals, so far as concerns the 
mean arterial pressure, has shown divergent results. Some investi- 
gators have reported a fall of the mean pressure; others but little 
change. The results seem to depend, at least in part, upon the 
cardiac strength of the animal in question — dogs bearing the lesion 
better than rabbits. As a rule, there is some fall of the mean 
pressure, the amount of which tends to vary with the duration and 
severity of the lesion. 

The arterial pressure is perhaps maintained in suddenly 
established aortic lesions by the vasomotor and cardiac reflexes 
which are engendered by stimulation of the endocardium, but 
the chief factor of compensation lies in the heart muscle itself. 
The mean pressure is maintained chiefly as the result of enlargement 
and hypertrophy of the left ventricle, which lead to an increased 
systolic output. 1 

The experiments of Stewart 2 indicate that much less blood actually 
regurgitates into the heart during diastole than is generally supposed. 
This is owing to the increased tonicity which the left ventricle 
assumes. The great difference between the systolic and the diastolic 
pressure which occurs has been attributed to a reflex lowering of 
the minimum pressure. The main fall of pressure is systolic in 
time, and is due to increased capillary flow. This is borne out by 
the fact that even in case of good compensation the diastolic press- 
ure may range between 40 and 60 mm. Hg., while the systolic 
pressure is about 180 mm. The tremendous pressure fluctuations 
to which the arteries are subjected is an important factor in the 
arteriosclerotic changes which the vessels undergo in these cases. 

Wiggers's 3 studies with optical manometers, however, indicate 
that the rapid systolic fall of pressure is not due to vasodilatation, 
since (1) the change occurs too rapidly (within a single beat), (2) 

1 Krehl, L., Pathologische Physiologie, 1910, p. 18. 

2 Experimental and Clinical Investigations of the Pulse and Blood-pressure changes 
in Aortic Insufficiency, Arch Int. Med., 1908, i, 102. 

3 The Dynamics of Aortic Insufficiency, Arch. Int. Med., 1915, xvi, 132. 



236 BLOOD-PRESSURE IN CARDIAC DISEASE 

it occurs even when the vessels have been previously dilated by 
means of nitroglycerin, and (3) the condition is enhanced rather 
than abated by epinephrin. 

He attributes the dynamic changes of aortic insufficiency to the 
fact that the initial interventricular tension is increased "owing to 
a regurgitation of pressure during diastole; this in turn causes a 
more vigorous ejection of a larger blood volume in the early portion 
of the next systole. This may be accompanied by an actual de- 
creased ejection during the latter portion of systole, thus, at once, 
accounting for the facts (a) that the systolic decline becomes steeper 
and (b) that the total systole output may not increase appreciably 
beyond the normal." 

Clinical Data. — The enormous pulse pressure which is frequently 
seen in aortic insufficiency with good compensation is often suffi- 
cient to alone establish a diagnosis. This finding is analogous to 
the other pulsatory phenomena which are so characteristic of this 
lesion. 

Landolfi, Roch, and others have reported circulatory hippus as 
a sign. It is generally manifest when the pulse is slow and the 
systole powerful (digitalis). Myosis corresponds with systole or 
increased pressure. 

A high systolic (180 to 200 mm.) associated with a low diastolic 
(GO to 30 mm.) pressure is strong presumptive evidence in favor 
of aortic regurgitation. In estimating the diastolic pressure by 
the auscultatory method the fourth phase must be chosen as the 
criterion, since the fifth phase often persists down to mm. This 
phenomenon is suggestive but not pathognomonic of aortic insuf- 
ficiency. A fall of pressure often indicates a failing ventricle. We 
should not speak of hypertension in cases of aortic insufficiency 
unless the systolic pressure exceeds 200 mm. 

The intensity of the diastolic aortic murmur in some cases 
increases with a rise of systolic pressure. A fall of pressure may 
cause a feeble murmur to become inaudible. The arterial sound 
heard in some cases in the femoral artery without aortic leakage 
depends to a considerable extent upon the pulse pressure, but 
especially upon the existence of an abnormally low diastolic pressure 
(Dehio).' 

Differences in the Blood-pressure in the Arm and Leg. — Under 
normal conditions the systolic pressures in the arm and leg of 
an individual lying quietly in a horizontal position are equal. 



AORTIC LESIONS 237 

When the erect or an inverted posture is assumed the pressures in 
the arm and leg "differ by the hydrostatic pressure of the column 
of blood which separates the points of the measurements. In 
these postures the pressure in the arteries of the leg varies greatly, 
while in the arm the pressure is kept about the same by the mechan- 
ism which compensates for the influence of gravity." In aortic 
insufficiency a great difference between the arm and leg pressures 
in the recumbent posture has been found (150 mm. Hg. higher 
in the leg) which is of diagnostic significance. It is most marked 
in uncomplicated and compensated cases and diminishes as soon 
as mitral insufficiency and dilatation of the right heart occur. 
Both fever and the application of hot water lessen the difference 
by relaxing arterial tone in the lower extremities, 1 in which the 
arteries are assumed to be in a contracted state in an effort to pre- 
vent cerebral anemia. 2 Another explanation of the higher leg press- 
ure is offered by Hill and Wells 3 who believe that it is due to a 
better conduction by the pulse wave in contracted and more rigid 
arteries. Hill 4 has recently stated that in addition to the just men- 
tioned factors the resonating effect (periodic vibration) of the 
abdominal cavity also plays a part. According to the latter con- 
ception " Resonation of the tissues must be held to play an important 
part in the transmission of the pulse, and thereby to save the work 
of the heart. The work of the heart we know is largely conserved 
by the elastic recoil of the arteries. But this elastic recoil of the 
arteries is aided by the resonance of the tissues. Every artery 
is in intimate relationship with its immediate neighbor. The pulse 
of one individual artery is aided by the pulses of the other arteries. 
The vigor of the circulation depends on the tone of the tissues, on 
the tautness of skin and muscle, and particularly of the abdominal 
wall. The hardened body of the trained athlete swings in full 
resonance with the pulse of his heart; the soft, flabby, ill-con- 
ditioned body of the sedentary worker offers a poor slack drum for 
his heart to thump." 

1 Rolleston, H. D., On the Systolic Blood-pressure in the Arm and Leg in Aortic 
Incompetence, Heart, 1912, iv, 83. 

2 Hill, Flack, and Holzman, The Measurement of Systolic Blood-pressure in Man, 
Heart, 1909, i, 73; Hill and Rowlands, Systolic Blood-pressure, Heart, 1912, hi, 219. 

3 Wells, Russell, and Hill, Roy. Soc. Proc, 1913, B. lxxxvi, 180; Hill and Flack, 
ibid., 365. 

4 Hill, McQueen, and Ingram, The Resonance of the Tissues as a Factor in the 
Transmission of the Pulse and in Blood-pressure, Proc. Royal Soc, London, 1914, 
lxxxvii, 255. 



238 BLOOD-PRESSURE IN CARDIAC DISEASE 

Cases Illustrating the Differences in Arm and Leg Pressures in Aortic 
Insufficiency as Compared with Other Cardiac Lesions. 

Blood-pressure. 
Brachial. Ext. malleolar. 

No. Diagnosis. Systolic. Diastolic. Systolic. Diastolic. 

1 Arteriosclerosis, chronic nephritis, car- 

diac hypertrophy and dilatation, em- 
physema of lungs, portal congestion 171 106 167 107 

2 Mitral and tricuspid insufficiency, car- 

diac dilatation, passive congestion of 

lungs, liver, kidneys, portal system 113 75 112 80 

3 Aortic obstruction and insufficiency, 

arteriosclerosis, mitral insufficiency, 

cardiac hypertrophy, etc. . . . 151 69 191 122 

4 Aortic obstruction and insufficiency, 

mitral insufficiency, arteriosclerosis, 

chronic nephritis, etc 173 71 190 95 

5 Cardiac hypertrophy and dilatation, 

aortic insufficiency 222 127 300 190 

In Cases 1 and 2 there was no aortic leakage. The arm and leg 
pressures in the recumbent position were approximately equal. 
In Cases 3 and 4 (definite aortic insufficiency) there were marked 
differences in pressure. In Case 5, aortic regurgitation was doubt- 
ful, but the large pulse pressure, as well as the arm and leg differ- 
ence, were strong evidence in favor of the existence of the lesion. 

Traube's Sign. — a double tone heard over the femoral vessels — 
occurs chiefly in aortic insufficiency, as does also Duroziefs sign — 
a double murmur heard as the result of stethoscopic compression 
of the femoral artery. Both of these phenomena are most marked 
when the pulse pressure is. large. The former is caused by sudden 
distention of the artery by the large systolic output and by the 
sudden distention of the femoral vein due to tricuspid insufficiency. 1 

Huchard found that in aortic insufficiency of rheumatic origin 
the systolic pressure was increased only moderately; the diastolic 
pressure was subnormal; while in cases of arteriosclerotic origin 
both phases were markedly elevated. These findings he attributed 
to the greater valvular damage in Group 1 and the coincident 
presence of renal lesions in Group 2. 2 

In pure aortic obstruction the systolic, the diastolic and the 
pulse pressures are generally slightly elevated, due in part to left 
ventricular hypertrophy and in part to general arteriosclerotic 
changes. The pulse pressure is small, and the pulse feels hard 
and small, being gradual both in onset and in disappearance. 

1 Schultz, W., Ueber d. Doppeltonbildung a. d. Cruralgefaessen, Deut. med. Woch., 
1905, xxxi, 2, 1381 ; Tice, T., Clinical Significance of Some Peripheral Signs of 
Aortic Insufficiency, Illinois Med. Jour., September, 1911. 

2 Huchard, H., and Amblard, La tension arterielle dans les insuffisances aortiques. 
Jour, de Practiciens, May 29, 1909. 



MIT UAL LESIONS 239 

Aortic Aneurysm. — Many cases of aortic aneurysm have a normal 
arterial pressure. According to Williamson/ blood-pressure tends 
to be higher in cases of simple aortic dilatation than in cases in 
which a distinct aneurysm is present. A pressure difference (5 
to 20 mm.) in the two arms is very commonly found, and occurs 
in about the same proportion of cases whether the innominate 
artery is actually involved or not. Differences amounting to 
30 mm. or more occur in about one-third of the cases and indicate 
aneurysm rather than simple dilatation or mediastinal tumor, which 
latter causes inequality of tension somewhat less frequently than 
does aneurysm. Small inequalities of pressure are of little practical 
diagnostic value. Unilateral differences of 10 mm. in the two arms 
without any constancy as to the side occurred in 20 per cent, of 36 
cases studied by Phipps. 2 They are common in arteriosclerosis. 
The administration of potassium iodid or the injection of sterilized 
gelatin, which often relieves pain, has no effect on arterial tension. 3 

Unilateral pressure differences may also be encountered in 
arteriosclerosis, in hemiplegia, and in cases of cervical rib. In the 
last-named condition lowering of the arm sometimes produces a 
demonstrable decrease in the pulse pressure. 

Increased blood-pressure, especially that which is due to sudden 
muscular strain is, next to disease of the elastic fibers of the arterial 
media, the most important factor in the production of an aneurism. 

Mitral Lesions. — In compensated mitral insufficiency arterial 
pressure is practically normal. The reestablishment of functional 
efficiency after an attack of broken compensation is, as was first 
pointed out by Sahli, not rarely associated with a diminution of 
blood-pressure. In mitral lesions this rule applies to both maximum 
and minimum pressures. The same phenomena occur to an even 
greater extent in the broken compensation which occurs in pul- 
monary emphysema. In aortic and arteriosclerotic lesions the 
fall of pressure is much less marked. These apparently paradoxical 
phenomena are due to the fact that during the period of insufficiency 
the resistance to arterial outflow is increased as the result of (1) 
C0 2 accumulation in the blood which produces peripheral vaso- 
constriction, and (2) owing to increased venous pressure. The 
physics of this phenomena are illustrated in the following diagram : 

The reservoir (H) is filled with water which escapes through 

1 Lancet, November 30, 1907. 2 Boston Med. and Surg. Jour., 1915, clxxiii, 476. 
3 Mackinnon, M., Arterial Pressure in Thoracic Aneurysms, British Med. Jour., 
October 4, 1913. 



240 



BLOOD-PRESSURE IN CARDIAC DISEASE 



P (the capillaries) by means of .1 (arteries). If the stopcock 
be wide open, water will rise in the standpipe M (pressure) to the 
point n. If the stopcock be partially closed (increased peripheral 
resistance) it will rise to in, and even with a diminished head in 
// (lessened cardiac power) it will still rise to o. 

A rise in the pulse pressure during symptomatic improvement is 
less constant, and when present it is more frequent in mitral lesions 
and in emphysema. This has been explained as due to the fact 
that under these circumstances the loss of compensation is the 
result of right heart weakness, the left heart being unaffected and 
being opposed by a greater peripheral tonus. With a constant 
blood-flow, aortic pressure and pulse pressure increase coincidently. 1 
The reestablishment of compensation must be associated with 
better cardiac filling and more forcible contraction. As soon as 



H 



s 



D 



Fig. 89. — Diagram illustrating the rise of arterial pressure which results from 
increased peripheral resistance. (After Lang and Manswetowa.) 



an improved circulation occurs, oxygenation of the blood is increased 
and peripheral spasm relaxes. 2 Several observers have constantly 
found that a temporary increase of pidse pressure occurs at the 
beginning of compensatory reestablishment. 

In compensated m%tral obstruction pressure is, owing to peripheral 
vasoconstriction, more often above than below the normal. The 
pulse pressure is small. Hypotension may therefore be of some 
value in diagnosticating between hemoptysis due to tuberculosis 
and that due to mitral obstruction. Marked persistent high 
pressure without edema generally indicates renal involvement. 

1 Furst and Soetbeer, Untersuchungen u. d. Beziehungen z\v. Fullung u. Druck 
m. d. Aorta, Deut. Arch. f. klin. Med., 1907, xc, 190; Strassburger, Ueber d. Einfluss 
d. Aoitenelastizitat a. d. Verhaltniss z\v. Pulsdruck u. Schlagvolumen d. Herzens, 
1907, Ibid., xci. 378. 

- Lang, G., and Manswetowa, S., Zur Frage d. Veranderung des arteriellen Blut- 
druckes l>ci Herzkrankheiten wahrend d. Kompensationsstorung. Deut. Arch. f. 
klin. Med., 190S. xciv, 455. (See Bibliography and numerous statements in the 
foregoing discussion.) 



MYOCARDIAL DISEASE 241 

Lagrange 1 found the arteriocapUlary pressure (as indicated by 
the sphygmomanometer of Bouloumie) in mitral stenosis higher 
than normal, the arterial pressure about normal. In eases asso- 
ciated with arteriosclerosis, pressure was distinctly elevated (180 
mm.), and in such cases a sudden fall was prognostically grave. 

Edema and Blood-pressure. — It has been suggested that edema 
increases blood-pressure by mechanically compressing the peripheral 
arteries, and that this plays a part in the increased pressure which 
is seen in broken compensation. If it ever plays any such part it 
must be a very insignificant one, since ordinarily edema and vascular 
tension bear no constant relation to each other. Pressure may 
either rise or fall while dropsy increases or diminishes. The occur- 
rence of edema in cardiac no less than in renal disease is not, as 
formerly supposed, merely a question of hemodynamics but is 
closely related to certain metabolic abnormalities, notably the 
retention of sodium chloride in the body. Experimentally pulse 
pressure bears a definite relation to edema and infarction. It has 
been shown that edema, which occurs readily in perfused organs, 
may be largely prevented if an intermittent — pulsating — pressure 
be employed. 2 Erythrocytic diapedesis occurs at the point at 
which pulsation of the arteries can no longer be seen. 3 

In uncomplicated valvular disease in which an increased pressure 
exists no effort should be made to lower tension by means of vaso- 
dilator remedies. Vasoconstriction is in these cases an effort to 
correct myocardial insufficiency by inciting the ventricles to 
restore the proper output (Starling). An increased pressure during 
compensation may be necessary to insure the requisite speed of 
capillary flow. 4 (See p. 285.) 

Myocardial Disease. — Much of what we have stated regarding 
arteriosclerosis and arterial hypertension applies to myocardial 
disease, because the latter generally is very frequently the terminal 
stage of the former. Since it is impossible to differentiate clinically 
between different forms of myocardial degeneration, they may be 
considered as a group. 

As in valvular lesions, blood-pressure in chronic myocardial 

1 Essai de Sphygmotonometrie clinique appliquee au diagnostic du retrecissement 
mitral, Arch. gen. de Med., 1908, excix, 293. 

- Hamel, Die Bedeutung des Pulses f. d. Blutstrom, Zeitsch. f. Biol., 1889, xxv, 474. 

3 Mall and Welch, Thrombosis and Embolism, Albutt's System of Medicine, 
1899, p. 254. 

4 Korke, V. T., Systolic Blood-pressure in Diseases of the Heart, Lancet, December 
2, 1911, p. 1547. 

16 



242 BLOOD-PRESSURE IN CARDIAC DISEASE 

disease is variable, although with the exception of the terminal 
stages, an increase will usually be found. The pulse pressure is 
often small. Such a finding is common even when functional 
capacity is far from good. In these cases exertion produces 
oppression, dyspnea, etc., and a fall of pressure (see page 152). 
Stewart found a slow blood-flow as low as 0.2 gm. per 100 c.c. 
per minute as compared with a normal of 3 to 5 to 14 gm. Not 
infrequently myocardial cases show a normal systolic but a high 
diastolic pressure. Rosenfeld 1 believes that a very low blood- 
pressure associated with mild anginal attacks, dilatation of the left 
ventricle and aorta, and auricular fibrillation especially if associated 
with a positive Wassermann reaction points strongly to syphilitic 
myocarditis. Salvarsan must be administered with caution in these 
cases owing to its tendency to lower blood-pressure and bring on 
tachycardia. The absence of hypertension and cardiac hypertrophy 
in syphilitic arterial disease was pointed out by Cautley. 2 

Extrasystolic Arhythmia. — The genesis of this form of cardiac 
irregularity may be closely associated with arterial tension. Both 
experimentally and clinically it is often induced by increasing 
arterial pressure and abated when. tension is diminished. When 
due to such a cause it may be interpreted as an indication that the 
heart is beginning to stagger under its burden. The extrasystoles 
themselves are less forcible than the regular contractions, and the 
ventricle is less well filled. Hence their systole pressure level is 
lower than that of the regular contraction. The postextrasystolic 
pressure is often higher — prolonged diastole. The existence of 
hypotension in association with extrasystoles, other things being 
equal, points to a purely functional origin of the arhythmia. 

Tachycardia. — Low blood-pressure is generally associated with 
tachycardia, especially in fevers. In such cases the hypotension 
may in part be responsible for the rapid pulse, although both 
symptoms are in the main result of toxemia. In paroxysmal 
tachycardia, there is, during the paroxysm, often a fall of the arterial 
and a rise of the venous pressure due to insufficient diastolic filling 
of the ventricles. 

Bradycardia is often accompanied by relatively slight blood- 
pressure changes. With a very slow pulse, however, the diastolic 
pressure is generally considerably below the normal. Gibson has 
reported heart block associated with a pressure of 270-80 mm. 

1 Ueber Syphilitische Myocarditis, Deut. med. Woch.. 1914, xl, 1044. 
2 Lancet, April 6, 1901. 



EXTRASYSTOLIC ARHYTHMIA 243 

Bradycardia is sometimes due to increased arterial tension. The 
latter condition produces central stimulation of the vagus, and this 
in turn a slowing of the pulse. When the hypertension is gradual 
in onset, an increased pulse rate is the rule, but when it is sudden, 
as occurs experimentally and in cases of acute nephritis, brady- 
cardia is more apt to result (Krehl). 

Pulsus Alternans. — A marked increase in pressure is the rule; in 
fact, this form of arhythmia, which is generally attributed to 
failure of ventricular contractility, may disappear with a fall and 
recur with a rise of arterial pressure. Herrick 1 finds the sphygmo- 
manometer useful not only in bringing out latent cases of pulsus 
alternans, but also in increasing the tactile perception of the alter- 
nation. The cuff is inflated to the point at which the pulse rate 
becomes halved. If the cuff pressure is allowed to fall somewhat 
lower all the beats will come through, but the alternation in their 
size becomes more noticeable than when the arterial lumen is 
uncompromised. 

Auricular Fibrillation. — In auricular fibrillation successive pulse 
waves are so extremely variable in both size and tension that it 
is not possible to draw any accurate conclusions from ordinary 
blood-pressure readings. The largest pulse waves are often 40 or 
50 mm. higher than the smallest. An approximate average pressure 
may be obtained, as suggested by Janeway, by noting the pressure 
of the largest and the smallest pulse waves separately, a method 
which emphasizes the number of waves which fail to come through 
at a certain pressure. Silberberg 2 employs a Mackenzie polygraph, 
upon which he records the pulsations of both radial arteries, one 
of them under increasing degrees of cuff pressure, thus obtaining 
a graphic record of the relative pressure of different systoles (Figs. 
89, 90, and 91. 

A more satisfactory method of estimating blood-pressure in 
auricular fibrillation has been suggested, based upon what is known 
as the relative pulse deficit. 3 

The pressure in the cuff which has been raised above the highest 
systolic pressure is allowed to fall 10 mm. at a time and interruptedly 
checked. A count is now made of the number of pulse waves which 
pass the cuff at a given pressure, in relation to the number of cardiac 
contractions as counted per minute over the precordium by an 

1 Jour. Am. Med. Assn., February 27, 1915. 

2 British Med. Jour., April 6, 1912. 

3 James, W. B., and Hart, T. S., Auricular Fibrillation; Clinical Observations on 
Pulse Deficit, Digitalis, and Blood-pressure, Amer. Jour. Med. Sci., 1914, exlvii, 63. 



244 BLOOD-PRESSURE IN CARDIAC DISEASE 



Fig. 90 



90 



100 



Fig. 91 



U0' 



130 



140 



Fig. 92 



Figs. 90, 91, and 92.— Three strips of tracing (right and left radial) taken from 
the same patient. Fig. 89, before brachial compression; all the beats come through. 
Fig. 90, the smallest beats xx disappear at a pressure between 90 and 100 mm. Hg. 
Fig. 91, the largest beats fail to record at a pressure of 140 mm. Hg. 





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Fig. 93. — The shaded area represents the pulse deficit; the upper edge is the 
apex rate; the lower edge is the radial rate. The broken line indicates the range 
of the "average systolic blood-pressure." Digitalis figures indicate minims of the 
tincture and dram of the infusion. October 13, admitted to hospital. November 
3, up in chair half an hour; November 9, up in chair two hours. December 4, up in 
chair four hours. At this time she had a crop of external hemorrhoids which caused 
much distress. (James and Hart.) 



EXTRASYSTOLIC ARHYTHMIA 245 

assistant. The excess of the latter over the former constitutes the 
"deficit.'" The process is repeated until all the beats traverse the 
cuff — until there is no deficit. 



Brachial 


pressure. 


Radial count. 


Apex count. 


140 mm. 





64 


130 


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50 


64 


120 


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110 


tt 


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In this cases there is no actual deficit, because below 100 mm. 
all the beats reach the periphery. But there is a relative deficit 
which occurs as soon as pressure is raised above 100 mm. 

The "average systolic pressure" is determined as follows: 

"The apex and radial are counted for one minute, then a blood- 
pressure cuff is applied to the arm, and the pressure raised until 
the radial pulse is completely obliterated; the pressure is then 
lowered 10 mm . and held at this point for one minute while the 
radial pulse is counted; the pressure is again lowered 10 mm. and 
a second radial count is made; this count is repeated at intervals 
to 10 mm. lowered pressure until the cuff pressure is insufficient 
to cut off any of the radial waves (between each estimation the 
pressure on the arm should be lowered to 0). From the figures 
thus obtained the average systolic blood-pressure is calculated by 
multiplying the number of radial beats by the pressures under 
which they came through, adding together these products and 
dividing their sum by the number of apex beats per minute. The 
resulting figure is what we have called the ' average systolic blood- 
pressure.' ' The following observation made on a patient will 
indicate the method of computation: 

B. S., April 29, 1910. Apex, 131; radial, 101; deficit, 30. 

Brachial pressure. Radial count. 

100 mm. 

90 " 13 13 X 90 = 1170 

80 " 47 - 13 = 34 X 80 = 2720 

70 " 75 - 47 = 28 X 70 = 1960 

60 " 82 - 75 = 7 X 60 = 420 

50 " 101 - 82 = 19 X 50 = 950 

Apex = 131)7220 

Average systolic blood-pressure 55 + 

Kilgore 1 has suggested the following method which is more 
accurate than that just described. 

1 The Fractional Method of Blood-pressure Determination, Arch. Int. Med., 
1915, xli, 939. 



246 



BLOOD-PRESSURE IN CARDIAC DISEASE 



The Fractional Method. — This method differs from that of James 
and Hart in the fact (1) that diastolic readings are made by deter- 
mining the fifth auscultatory phase and, (2) by a different interpre- 
tation of the systolic readings. 



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50 60 



80 PER MIN. 



Fig. 94. — Showing the relation of systolic and diastolic pressures in a typical 
case of auricular fibrillation in which the diastolic pressure of one cycle never exceeds 
the systolic pressure of another. The numbers at the left indicate millimeters of 
mercury pressure in the pneumatic cuff; those at the bottom the rate per minute of 
beats counted in various ways. The upper line here represents the results of palpa- 
tory systolic counts, the lower line fifth phase diastolic counts. 



These readings are made at 5 instead of 10 mm. Hg. intervals, 
and are tabulated as having an average value of 7.5 mm. Thus in 
a given case with 88 pulse beats per minute and a pressure ranging 
between 110 and 145 mm 
obtained. 



the following chart and figures were 



PRACTICAL CONSIDERATIONS 247 



(a) (6) • (c)> 








6-0=6 


6 X 147.5 = 885 






8-6=2 


2 X 142.5 = 285 






14 - 8 = 6 


6 X 137.5 = 825 






38 - 14 = 24 


24 X 132.5 =3,180 






60 - 38 = 22 


22 X 127.5 = 2,805 






70 - 60 = 16 


16 X 122.5 = 1,960 






82 - 76 = 6 


6 X 117.5 = 705 






88 - 82 = 6 


6 X 112.5 = 675 


r88 






11,320 H 


= 128.6 = average 








systolic pressure. 



Lewis, 2 who experimentally investigated the effect of auricular 
fibrillation upon the circulation as a whole, found that blood- 
pressure, while it might rise or fall or remain unchanged, generally 
fell, soon to regain its original level. The volume of the intestines 
behaved in a similar manner; the venous pressure in just the 
opposite manner. From these experiments it appears that auricular 
fibrillation does not necessarily entail any marked changes on the 
circulation as a whole. In human disease, however, we are dealing 
not only with an arhythmia but with a diseased myocardium as well, 
so that marked differences are readily accounted for. 

Doubtless part of the blood-pressure variations which occur 
in association with various forms of aryhthmia are the result 
of mechanical respiratory influences. While Henderson has 
emphasized that heart rate changes in man have an important 
part in blood-pressure variations, and while in some cases they 
are the only determining influence, yet this is, according to Wiggers, 3 
not the only nor even the main factor in the majority of cases. 

Practical Considerations. — Blood-pressure observations are often 
distinctly useful in the diagnosis of valvular lesions. A high systolic 
and a low diastolic pressure suggests aortic insufficiency, the 
murmur of which is often low pitched and easily overlooked. If 

1 In the figures shown herewith the numbers on the base line correspond to the 
figures in column a in the above tabulation; i. e., they represent total numbers of 
waves felt or sounds heard at the corresponding cuff pressures. For some purposes 
it would be an advantage to construct curves in which the base line figures repre- 
sented the quantities in column c, i. e., the number of beats which have a certain 
pressure. In such a figure taken from a normal case there would be two narrow 
curves separated by the amount of the pulse pressure, while if it were from a very 
irregular case the diastolic and systolic curves might overlap. The work of construct- 
ing these additional curves is unnecessary if it is remembered that their lateral extent 
would depend on the slope of the curves here employed. In the figures herewith, 
the more uniform the pressure of the beats, the more nearly horizontal the lines, 
and the more variable the pressure the more sloping the lines. 

2 Fibrillation of the Auricles, its Effect upon the Circulation, Jour. Exp. Med., 
1012, xvi, 395. 

3 Does Cardiac Rhythm alone Determine Blood-pressure Variations? Jour. Exp. 
Med., 1914, xix, 1. 



248 BLOOD-PRESSURE IN CARDIAC DISEASE 

a double aortic murmur is heard, blood-pressure readings will often 
help us in deciding whether the obstruction or the insufficiency 
is the preponderant lesion. In aortic obstruction the pulse pressure 
is small. Again, in case of a presystolic murmur associated with 
an aortic lesion the sphygmomanometer may help us in deciding 
whether we are dealing with a Flint murmur or with an additional 
mitral obstruction. In the latter case the pulse pressure is small 
and the systolic pressure relatively normal. 

In cases presenting the symptoms of angina pectoris a high 
blood-pressure is evidence in favor of an organic lesion, although 
the occurrence of a normal pressure by no means excludes it. Well- 
marked hypotension in patients complaining of weakness and 
vertigo with dyspnea on exertion, points to a loss of vasomotor tone 
rather than to a myocardial lesion in which pressures are generally 
normal or slightly increased. 

Many cardiac murmurs in advanced life are due to roughening 
and sclerosis of the valves, although their actual functional capacity 
may be but little impaired. Here, again, the absence of significant 
pressure abnormalities may help in solving the problem. Some 
light may also be thrown upon the strength of the heart muscle 
by the duration of the different auscultatory phases (see page 68). 
A certain amount of the increased tension seen in cardiac patients 
is due to their psychic state (discomfort, anxiety, fear, etc.). Jane- 
way has suggested that a dose of morphin, which is often followed 
by marked and often lasting improvement in such cases, may 
also show how much of the increased pressure is due to the mental 
condition. 

Pericardial Effusions. — It has been known ever since the experi- 
ments of Cohnheim that a rise of intrapericardial pressure is followed 
by a decreased aortic pressure, and vice versa. 

Experimental Data. — Under normal circumstances the peri- 
cardium — which is in health indistensible and capable of with- 
standing a pressure sufficient to rupture the myocardium — acts as 
a protective covering to the heart under conditions of strain. It 
prevents cardiac dilatation beyond a certain point and in so doing 
adds measurably to the efficiency of the tricuspid valve. 1 It pre- 
vents the further inflow of venous blood when a certain stage of 
dilatation has been reached, which, did it not occur, would lead 
to interstitial hemorrhage and myocardial rupture. 2 It has been 

1 Barnard, Proc. Jour. Physiol., 1S98, xxii, p. 43. 

- Kudo, V., The Significance of the Pericardium, ibid., 1915. p. 1. 



BRONCHIAL ASTHMA , 249 

shown that when the heart of a curarized animal (cat) is enclosed 
in a glass canliometer very small changes of pressure in the cardi- 
ometer system produce comparatively wide changes in the carotid 
pressure. Thus, an increase of 1 mm. Hg. of extracardial pressure 
caused a fall of 8 mm. in the systolic pressure. These changes 
occur within the space of time occupied by two heart beats. If 
intrapericardial pressure is raised with the heart in situ essentially 
similar results are obtained 1 (see page 41). 

Clinical Data. — In pericardial effusions we therefore find a lowered 
arterial tension and a decreased pulse pressure. Owing to the in- 
creased intracardial pressure, less blood reaches the right auricle, 
the blood-flow into which is normally abetted by the fact that 
extrathoracic pressure is higher than that in the venae cava?. Hence 
a smaller volume of blood reaches the left ventricle; and since the 
systolic output is decreased, arterial pressure must fall unless 
these effects are counterbalanced by a peripheral vasoconstriction. 
These same causes produce an increased venous pressure which 
is compensatory in nature; for if venous pressure were to fall below 
intracardial pressure no blood would reach the right auricle. Intra- 
thoracic pressure being lower during inspiration and higher during 
expiration, it is evident that when venous and intrapericardial 
pressures are nearly equal the act of breathing will have an alter- 
nately inhibiting and accelerating effect upon the blood-flow to 
the heart, which results in the pulsus paradoxus — decreased volume 
during inspiration. For the reasons just stated, this phenomenon 
only occurs at a certain stage (broken compensation), and in certain 
cases of pericardial effusion. 2 

Bronchial Asthma. — Asthmatic attacks are nearly always accom- 
panied by hypertension. This may result from (1) asphyxia or 
(2) complications, especially nephritis. The act of coughing produces 
a temporary marked increase of tension which is coincident with 
the expiratory movement. 

1 Lewis, Th., The Influence of Intrapericardial Pressure upon the Inspiratory 
Rise of Blood-pressure in Vagotomized Cats, Jour. Physiol., March 21, 1908, xxxvii. 

2 Calvert, W. J., Pulsus Paradoxus in Pericarditis with Effusion, Jour. Anier. 
Med. Assn., 1907, xlviii, 1168. 



CHAPTER XI. 

BLOOD-PRESSURE IN ARTERIOSCLEROSIS— VASCULAR 

CRISES. 

About one-third of all cases of well-marked peripheral arterio- 
sclerosis have normal or subnormal pressures. In the remaining 
two-thirds the pressure is variably increased, depending mainly 
upon the degree of renal involvement. Arteriosclerosis is selective in 
its location; thus syphilis attacks the ascending aorta. Individuals 
who perform severe physical labor often develop peripheral vascular 
lesions of extreme degree, yet the pipe-stem radial artery is often 
a relatively benign type of the disease. Savill's 1 investigations 
based on 400 autopsies on individuals of and over sixty years of 
age, showed that extensive patchy atheroma is consistent with 
extreme longevity, with an entire absence of symptoms or vascular 
complications. This same statement is applicable to marked 
generalized intimal and adventitial sclerosis so long as the medial 
arterial wall is relatively uninvolved. The foregoing statements 
are borne out by Ophiil's studies, 2 who failed to find cardiac hyper- 
trophy in 35 per cent, of all cases of marked arteriosclerosis. 

The hypothesis advanced by Hasenfeld and Hirsch that arterio- 
sclerosis is unaccompanied by increased blood-pressure unless the 
arterioles in the subdiaphragmatic and splanchnic domain are the 
seat of disease has caused much discussion and is now not generally 
accepted. Sclerosis of either the large or the small splanchnic 
vessels is not a common finding. A spastic condition of these 
vessels may exist, however, which will increase tension, although 
this is not apt to occur once the vessels are definitely sclerotic. 

Longcope and McClintock 3 found that compression of the 
superior mesenteric artery and the coeliac axis gives rise constantly 
to an elevation of blood-pressure which may last for at least an 
hour. This rise of pressure is mechanical, due not to a reflex action 

" Lancet, 1904, p. 506. 

2 Subacute and Chronic Nephritis as Found in One Thousand Unselected Autop- 
sies, Arch. Int. Med., 1912, ix, 158. 

3 The Effect of Diminished Blood Supply to the Intestines upon the General 
Circulation, Johns Hopkins Med. Bull., 1910, xxi, No. 234. 



BLOOD-PRESSURE IN ARTERIOSCLEROSIS 251 

but to an increased amount of blood in the general circulation. 
The pressure remains increased until the excess of blood accumulates 
in the ramifications of the splanchnic vessels by way of collateral 
anastomosis. But even if this constriction is maintained for several 
months in dogs neither hypertension nor cardiac hypertrophy 
develop. 1 This may be due to the compensatory effect of an efficient 
collateral circulation. Furthermore, Marchand 2 was unable to 
establish any definite relationship between cardiac hypertrophy 
and the degree of arteriosclerosis of the abdominal aorta or the 
splanchnic vessels. 

The evidence now at hand points strongly to the view that 
hypertension when present in arteriosclerosis is due to sclerosis 
of the systemic arterioles. While, therefore, the dictum that a 
man is as old as his arteries still holds good, yet it appears that 
the condition of the smallest arteries is more important than the 
largest ones; and, further, we are not justified in assuming that 
because the radial artery shows extensive disease, the more vital 
arteries and arterioles are therefore correspondingly involved. 

The causes and pathology of vascular disease cannot be discussed 
here, and only the phases of the problem which have a distinct 
bearing on blood-pressure will be considered. 

Osier states that (1) high blood-pressure is one of the causes of 
arteriosclerosis — the others being (2) wear and tear, (3) infections 
and (4) intoxications. The following classification of arteriosclerosis 
has been suggested by Allbutt: (1) Toxic: plumbism, diabetes, 
infectious diseases, notably syphilis; (2) involutionary, from 
senile degeneration; (3) secondary, following hypertension. Clinic- 
ally, such changes are manifested by arterial hypertension, cardiac 
hypertrophy, albuminuria, and varying subjective phenomena; the 
first of these resulting from tonic contraction of the arterioles and 
capillaries. With prolonged increase of pressure the systemic 
arteries at first become thickened and hypertrophied. The cerebral 
vessels and the aorta being less liberally endowed with muscular 
tissue dilate, and, either with or without aneurysmal change, not 
infrequently rupture. The vascular damage in these cases is largely 
mechanical, as in occupations associated with hard labor; whereas 
arterial degeneration in the organs, especially the kidneys, results 
mainly from toxic irritation. As a rule arteriosclerosis is unasso- 

1 The Effect of Permanent Constriction of the Splanchnic Arteries and the Asso- 
ciation of Cardiac Hypertrophy with Arteriosclerosis, Arch. Int. Med., 1910, vi, 439. 

2 Verhandl. Kong. f. inn. Med., 1904, xxi, 60. 



252 BLOOD-PRESSURE IN ARTERIOSCLEROSIS 

ciated with arterial hypertension. The blood-pressure in arterio- 
sclerosis is of course higher than in youth, but the degree and the 
constancy of the elevation depend chiefly upon the location and 
character of the arterial changes, and sometimes upon the extent 
to which the splanchnic and renal arterioles are affected. Extensive, 
spontaneous and often unexplainable variations of pressure are of 
frequent occurrence. 

Blood-pressure in Old Age. — In a study of 250 blood-pressures 
in the aged, Wildt 1 measured the systolic pressure according to 
Riva-Rocci; the diastolic according to Ehret. After sixty and up 
to ninety years of age there is a rise of pressure (averaging 137 and 
162 mm. respectively). After ninety years the systolic pressure 
gradually falls. Higher values were found in women than in men. 
Only after eighty years are equal values found in the two sexes. 
Factors of hypertension are arteriosclerotic processes, or minor 
grades of interstitial nephritis; occasionally high-grade interstitial 
nephritis. The diastolic pressure is relatively low and does not keep 
pace with the increase in the systolic element, thus differing from the 
readings obtained in hypertensive cardiovascular disease. The 
pulse pressure is apparently dependent on the amount of sclerosis 
of the aorta, as well as upon the degree of cardiac weakness. 

The findings illustrate what has been stated, i. e., that arterio- 
sclerosis per se does not, as a rule, produce much elevation of 
pressure, and that pressures exceeding 160 mm. Hg. over prolonged 
intervals of time are usually attributable to other causes, especially 
chronic nephritis. 

The great discrepancy in blood-pressure findings in arterio- 
sclerotic cases is largely due to the different classes of patients 
from which statistics have been drawn. In public hospitals the 
cases are generally not seen until symptoms have become urgent, 
and often not until a terminal fall of tension has occurred; whereas 
cases observed in private or consultation practice among the 
well-to-do classes are seen during and at the beginning of the 
high-pressure period, the " presclerotic" stage of Huchard. 

Vascular Reactions in Arteriosclerosis. — The circulation in 
arteriosclerosis differs in many ways from that in health. The 
normal arm, according to O. Midler's plethysmography studies, 
contains about 7 per cent, of blood; in arteriosclerosis this amount 
is much decreased. Abnormal local variations in blood-pressi/re, 

1 Ueber Blutdruok im Greisenalter, Zentralbl. f. Herz. u. Gefasskrankh.. 1912, 
iv, S. 41-49. 



VASCULAR REACTIONS IN ARTERIOSCLEROSIS 253 

either unilateral or bilateral, in corresponding or different regions 
of the body are not uncommon in arteriosclerosis. 

In the case of normal arteries the fall of pressure in passing from 
the aorta to the periphery is gradual. The first important fall 
occurs in the capillaries. In sclerotic vessels, however, vascular 
contraction of the arterioles and small arteries is capable of pro- 
ducing well demonstrable pressure differences in homologous 
peripheral arteries. Findlay 1 found that as the age of the subject 
increased there was constantly increasing tendency for marked 
pressure variations to occur between the central and peripheral 
arteries, e. g., brachial and digital. In the majority (80 per cent.) 
of the cases, the proximal vessel showed the higher pressure. These 
findings were especially noticeable in cases of arterial hypertension 
and are apparently due to arterial contraction. 

This fact has been emphasized by Teissier, 2 who believes that 
these localized inequalities of pressure indicate the site of the 
arteriosclerotic process. Thus, if the splanchnic vessels are chiefly 
affected, hypertension is said to occur in the dorsalis pedis artery, 
while increased tension in the temporal or the radial arteries points 
respectively to involvement of the intracranial or the intrathoracic 
vessels. This he explains as due to a segmental phenomenon to 
which the peripheral and the deep-seated arteries react similarly. 
In one case increased pressure in the temporal artery was soon 
followed by the appearance of glaucoma on the same side. In 
another case a similar pressure increase preceded attacks of facial 
paralysis, vertigo, and apoplectiform manifestations. 

These observations are of great interest but must be accepted 
with considerable reserve on account of the possibility of instru- 
mental error. The normal pressures as obtained with the Potain 
apparatus, which Teissier used, are 16 to 18 cm. in the radial, 13 
to 15 cm. in the dorsalis pedis, and 8 to 12 cm. in the temporal 
arteries. Even if careful allowances are made for postural varia- 
tions, the unavoidable margin of error would often be greater than 
the actual supposedly abnormal pressure variations. (See also 
under Functional Tests.) 

Inequality of the pressure of the pulse on the two sides of the 
body (5 to 15 mm.), if constantly present and not attributable to 

1 The Systolic Pressure at Different Points of the Circulation in the Child and the 
Adult, Quart. Jour. Med., 1910, iv, 489. See also Pesci, Riforma Medica, June 7, 
1909. 

2 Role des Hypertensions partielles dans les determinations symptomatiques de 
l'arteriosclerose, Bull. d. l'Acad. de Med., February 25, 1908, lxxii. 



254 BLOOD-PRESSURE IN ARTERIOSCLEROSIS 

any local abnormality, often, points to arteriosclerotic changes. 
Engel 1 believes that this sign may be useful in diagnosticating 
between primary nephritis and arteriosclerosis. (See Aortic 
Aneurysm.) 

Disproportionate hypertension of the arteries of the lower 
extremities has been described by Teissier as a constant phenomenon 
in abdominal aortitis. Recent observations of Pierret made with 
the Pachon apparatus on the pressures of the radial and tibial 
arteries have shown in 17 out of 20 cases higher readings in the 
lower limb (30 mm. systolic, 10 mm. diastolic). Heitz 2 found that 
the arm and leg readings differ very considerably, depending on 
the size of the cuff employed and whether the Pachon or the Riva- 
Rocci instruments are used. 

The rapidity of transmission of the pulse wave depends upon both 
the condition of the vascular wall and to a less extent upon the 
height of blood-pressure. The normal rate is 8.3 to 12 m. per 
second. In arteriosclerosis the rate has been found increased to 
10.1 m. (Friberger, 3 ), 23 m. (Miinzer). 4 In dicrotic pulses the trans- 
mission is delayed. This rapid transmission of the pulse wave, 
associated with a relatively low diastolic pressure often leads one to 
overestimate the vigor of the pulse. The rapidity of pulse trans- 
mission in different valvular defects depends far more upon the 
degree of tension and of arteriosclerosis than upon the character 
of the lesion. 5 (See Aortic Insufficiency, p. 235). 

The Nitrite Test.; — Rzentkowski 6 found in healthy subjects only 
a slight and brief diastolic fall after the inhalation of amyl nitrite. 
In arteriosclerosis, on the other hand, much greater and more 
prolonged lowering occurred despite increased cardiac activity. 
He interprets these facts as indicating that the splanchnic vessels 
have lost their compensatory contractility, which in normal individ- 
uals prevents much disturbance of tension. Arteriosclerotic hyper- 
tension may therefore (since the peripheral vessels still retain 

1 Berlin, klin. Woch., September 20, 1909, xlvi. 

2 Des Mensurations de Pression dans les Arteres des Membres Inferieures, Archiv. 
des Maladies du Cceur des Vaisseaux et du Sang, April, 1913, p. 285. 

3 Pulswellengeschwindigkeit bei Arterien m. fuhlbarer Wandverdickung, Deut. 
Arch. f. klin. Med., 1912, cvii, 280. 

4 Die Fortpflanzungsgeschwindigkeit der Pulswellen in Gesunden u. krankhaft 
veranderten Blutgefassen, Kong. inn. Med., 1912, xxix, 431. 

6 Beitriig z. Lehre v. d. Fortpflanzungsgeschwindigkeit d. Pulswellen b. gesunden 
u. kranken Individueu, Samml. wiss. Arb. 1, Langensalze, Wendt and Klauwell, 
1912, p. 39. 

6 Untersuchungen u. d. Wirkung des Amylum nitrosuni auf d. gesunde u. sklero- 
tische Arteriensystem, Zeit. f. klin. Med., 1909, xlviii, 111. 



VASCULAR REACTIONS IN ARTERIOSCLEROSIS 255 

their power of dilating) be regarded as due to prolonged organic 
splanchnic contraction. Whether this explanation be correct or 
not the practical procedure may be of some value as a test of 
arterial functionation. F. Franck states that permanent hyper- 
tension cannot be due to vasoconstriction, a muscular spasm which 
he believes cannot persist indefinitely. He calls attention to the 
fact that vasoconstriction in one locality is sooner or later always 
counterbalanced by vasodilatation elsewhere. 

The Stasis Reaction. — The blood-pressure is taken in the recum- 
bent posture by the auscultatory method. Following this, the 
circulation in three extremities is occluded by inflation of rubber 
cuffs. This procedure in normal individuals when maintained for 
five minutes usually produces a rise of pressure of from 5 to 10 
mm. Hg. In arteriosclerotics the usual average reaction is 27 
mm., the maximum 60. An increase of pressure under these 
circumstances, therefore, points to arteriosclerosis. Its absence 
does not exclude this condition (Hertzell). 1 

In cases of hypertension due to fibrosis of the arterioles a marked 
rise of pressure (50 to 60 mm. Hg.) occurs; if the increased press- 
ure is due to spasm of the arterioles the rise of pressure is less 
(15 to 20 mm. Hg.) as well as more transient in character (Hare). 

The Ice Reaction. — Romberg and his pupils have shown that the 
application of ice to the arm normally produces a diminished local 
blood-flow. In arteriosclerosis this reflex tends to be abolished. 
A merely hypertrophic artery may, however, show a normal or 
even an increased response. (See under Function Tests, page 173.) 

The Arteriocapillary Pressure Index. — Fink 2 maintains that there 
is a definite and characteristic relationship between arterial and 
capillary pressure in arteriosclerosis. If an index is established 
thus : 

arterial pressure _ 17-18 cm. Hg. (Potain) 
capillary pressure 9-10 cm. (Gaertner) 

the quotient will lie normally between 1.5 and 2. According to 
Fink we obtain in arteriosclerosis an index below 1.5, sometimes 
below 1. The smaller the quotient the more marked the evidences 
of circulatory insufficiency — dyspnea, edema, etc. But he specific- 
ally asserts that this is an index of circulatory efficiency and not 



1 Die Stauungsreaktion bei Arteriosklerose, Berlin, klin. Woch. ,1913, 1, S. 535-538. 

2 Nouvelles recherches sur la valeur, du rapport des tensions arterielles et capillaires 
dans l'arteriosclerose, Rev. de Med., August, 1908, p. 747. 



256 BLOOD-PRESSURE IN ARTERIOSCLEROSIS 

one of anatomic integrity. These observations would have more 
value if the factor of instrumental error could be reduced. 

In normal individuals the local application of heat to the hand 
produces a fall of the brachial and a rise of the digital pressures. 
In arteriosclerotics negative or atypical reactions are generally 
observed (Dobrymin) . 

VASCULAR CRISES. 

The term vascular crises was coined by Collier. The subject has 
been elaborately studied by Pal 1 and others, who class under this 
heading conditions which result from local or general (1) vaso- 
contraction, (2) vasodilatation, which arise without demonstrable 
anatomic lesions, the symptoms thus produced disappearing when 
normal vascular relations are reestablished. 

It is a self-evident fact that vasomotor stability, control, and 
compensation are among the most fundamental attributes of the 
animal economy. Furthermore, these intervascular relations must 
be adjusted and balanced to an extreme point of sensitiveness and 
delicacy. It is not surprising when one considers these facts that 
vasomotor incoordination should occur, especially under certain 
conditions which appear to predispose to it. 

It has been clearly established that certain vascular domains 
are controlled by definite vasomotor centres, as the mesenteric 
vessels by the splanchnic nerves. It furthermore appears likely 
that the enervation of such a system may be disturbed in part 
after the manner of segmental distribution, and also that the dis- 
turbances may be limited to the vasomotor element alone. There 
exists also a definite reciprocal relationship between certain vascular 
areas, by virtue of which a contraction in one produces a dilatation 
of the other. This phenomenon has been ascribed by some to active 
vasodilatation, by others to a purely mechanical displacement of 
blood. A vascular crisis may be brought about by an abnormal 
(1) contraction, or (2) dilatation, in a given vascular domain, which 
results in a certain train of direct or indirect symptoms which may 
manifest themselves in the immediate neighborhood or at a distance 
from the seat of the vascular abnormality, or in general vascular 
phenomena. Certain conditions appear to predispose to such 
vascular crises, notably arteriosclerosis, nephritis, pregnancy, 

1 Gefiisskrisen, Leipsic, 1905. 



VASCULAR CRISES 257 

tabes, and plumbism. The actual symptoms produced will depend 
upon (1) the vascular domain involved; (2) whether vascular spasm 
or dilatation exists; (3) whether these changes are compensated 
for in other vascular domains; (4) to what extent the function of 
the part or organ is affected, etc. The existence of local vascular 
crises has been indubitably demonstrated in spasmodic contraction 
of the central retinal artery (see page 409). 

I. Crises due to Vasoconstriction. — (a) The pectoral type, (6) 
the abdominal type, (c) the cerebral form, (d) the crises of the 
extremities (peripheral form), (e) the general vascular type, (/) 
paroxysmal dyspnea. 

The exact cause and mechanism of these vascular abnormalities 
is not easy. to determine. It cannot be sought primarily in the 
anatomical abnormalities of the arteries in question, because the 
spastic phenomena are often manifested in vascular areas which 
are not essentially diseased or primarily affected. It may be (1) 
that stimuli which arise in the diseased area exert their influence 
upon other domains; (2) that the sympathetic system is called into 
play by local abnormalities in the vaso vasorum; or (3) that some 
pressor substance gains entrance into the blood-stream. 

Angina Pectoris. — Although there is still much doubt regarding 
the genesis of angina pectoris, there can be no uncertainty that 
many if not all cases are closely allied to vascular spasm. Whether 
such a contraction is purely local — limited to the coronary arteries 
thus causing ischemia of the myocardium or whether it be of a 
more general nature, cannot be definitely stated. Angina pectoris 
is sometimes associated with Raynaud's disease and intermittent 
claudication, both of which are typical examples of local vascular 
spasm. The writer was on one occasion taking a blood-pressure 
reading during which an attack of angina occurred. The systolic 
pressure, previously 160 mm. Hg., suddenly rose to 210 mm. and 
remained at that point for the few minutes during which the pain 
lasted. In many cases of angina, however, the pressure during 
attacks is either normal or actually lowered. The latter occurs 
especially in the syphilitic cases and is what one should expect if 
coronary arterial spasm is accepted as the cause of the attacks. It 
is also to be remembered that both pain and anguish have potent 
pressor actions and that a rise of pressure when present may be the 
result and not the cause of the paroxysm. 

Anginal attacks may be preceded by or associated with evidences 
of local peripheral vascular crises — pallor, coldness, cyanosis. "It 
17 



258 BLOOD-PRESSURE IN ARTERIOSCLEROSIS 

is probable that by disease of the aorta its sensitive endowments, 
those which regulate blood-pressure, are disordered — exalted or 
impaired; and, during or near the attack, pain, dread or distress 
make all measurements of blood-pressures untrustworthy." 1 Tran- 
sient aphasia, paralysis, dead fingers," etc., which are also angio- 
spastic phenomena, may also occur coincidently with the paroxysms. 2 
Furthermore, angina pectoris and abdominalis may be alternately 
present in the same patient, and the symptoms of the latter are 
closely analogous to the abdominal vascular crises of plumbism, 
locomotor ataxia, angioneurotic edema, and purpura. Curschmann 3 
has reported cases illustrating the development of angina pectoris 
upon a basis of or as an accompaniment to peripheral vasomotor 
cramps, emphasizing the fact that the heart is embryologically 
only a specialized artery, so that its connection with the arteries 
is both anatomic and nervous. 

The subjects cf angina pectoris are the subjects of arterial 
disease — aortic, coronary, or general- — and sclerotic arteries readily 
exhibit spastic manifestations. Most of these patients have pre- 
viously had arterial hypertension for variable periods. During 
the paroxysms the pressure suddenly, markedly, and rapidly 
increases. While the rise may be abetted by the pain it is certainly 
not primarily caused by it, and it is often relieved by amyl nitrite. 
"In many cases the attack begins directly as a peripheral vaso- 
constrictor storm, with cold hands and cold feet, pallor of the face, 
and sweating. Nor is this simply in the so-called functional type, 
but in the severest forms an emotional disturbance may initiate a 
wide-spread contraction of the arteries. During the paroxysm it 
is by no means uncommon to find the radial pulse on one side 
much smaller than on the other" (Osier). 

Many but not all cases of angina pectoris show marked hyper- 
tension (190 to 220 mm.). The presence of increased pressure is 
often the best indication of an organic lesion, but its absence (150 
to 160 mm.) cannot be accepted as evidence of a mere functional 
or digestive disturbance. The following table shows the blood- 
pressure findings in cases of angina pectoris seen by the writer 
in private and consultation practice : 

1 Allbutt, C, Diseases of the Arteries Including Angina Pectoris, London, 1915, ii, 
338. 

2 Osier, Sir William, Angina Pectoris, Lancet. March 12 and 26, and April 9, 1910. 

3 Deut. med. Woch., 1906, xxxii, 38. 



VASCULAR CRISES 259 



No. 


Age. 


Blood 


-pressure. 


Outcome. 


1 


72 


185 ; 


and 


75 


Death in paroxysm. 


2 


73 


200 


" 


115 


Death in paroxysm. 


3 


19 


140 


" 


100 


Death from rupture of ventricle, 


4 


60 


160 


" 


110 


Unknown. 


5 


06 


200 


" 


130 


Unknown. 


6 


68 


138 


" 


120 


Unknown. 


7 


42 


200 


" 


110 


Unknown. 


8 


58 


200 


" 


165 


Death in paroxysm. 


9 


59 


190 


" 


100 


Unknown. 


10 


53 


150 


" 


100 


Living, free from symptoms. 


11 


70 


195 


" 


100 


Death in paroxysm. 


12 


68 


195 


" 


85 


Death in paroxysm. 


13 


62 


225 


" 


170 


Death from apoplexy. 


14 


72 


160 


" 


? 


Death sudden, third attack. 



Angina abdominalis — the abdominal counterpart of angina 
pectoris — is more or less closely associated with the clinical picture 
of abdominal arteriosclerosis. It is based upon the presence of 
periarteritis, local thrombosis, or vascular spasm of the mesenteric 
artery, and has been regarded as an intermittent dysperistalsis 
(Schnitzler, Ortner). The clinical manifestations consist of local 
abdominal pain, tenderness, tympanites, and of hypertension. 
Spasm of the iliac or femoral arteries leads to intermittent 
claudication. Disproportionately increased femoral blood-pressure 
has been described by French authors in association with acute 
abdominal aortitis. 

Paroxysmal epigastric pain in arteriosclerotic subjects is not 
uncommon and frequently results from organic changes in the 
gastro-intestinal tract. These attacks are sometimes brought on 
by overexertion, overeating, emotional disturbances, or by lying- 
down. 

Buch 1 distinguishes two classes of arteriosclerotic abdominal 
pain: (a) abdominal cramp; (6) angina abdominalis. The clinical 
manifestations of the former, tympanites, constipation and pain, 
are associated with autopsy findings indicative of intestinal paresis, 
due to ischemia. In angina abdominalis the pain may begin in 
the epigastrium and remain localized there. 

Paroxysmal dilatation of the abdominal aorta is a condition which 
occurs chiefly in run-down, emaciated, neurasthenic women with 
ptosis of some or all of the abdominal organs. The condition is 
characterized by an abrupt forcible pulsation of the abdominal 
aorta, which is objectively visible and of which the patient is 
subjectively conscious. Associated with this there may be vomiting, 

'St. Petersburger med. Woch., 1904, xxix, No. 27; Arch. f. Verdauungskrankh., 
1904, x, 6. 



260 BLOOD-PRESSURE IN ARTERIOSCLEROSIS 

epigastric pain, and sometimes faintness. The condition may slightly 
simulate aneurysm. The attacks end as suddenly as they begin, 
the termination being associated with the disappearance of pain 
and empty feelings in the epigastrium. They may last hours or 
days and during the attack blood-pressure generally is elevated 
30 or 40 mm. Between paroxysms pressure is normal. 1 

Tympanites. — The subjects of cardiovascular disease complain 
greatly of tympanites. Not only is flatulence a frequent symptom 
among them, but very slight degrees of distention cause a dispro- 
portionately great amount of discomfort. How often the subject of 
angina pectoris complains only of his "stomach"! 

The subject is complex. Undoubtedly vagus effects are account- 
able for both conditions, but it is further clear that abdominal 
distention mechanically interferes with heart action. Further, 
Stadler and Hirsch 2 showed experimentally that inflation of the 
bowel from the rectum causes a marked rise in blood-pressure. 
This may be due to a hindrance of the abdominal venous circulation, 
but more probably results from dyspnea, as it occurs coincidently 
with the rise of the diaphragm and fails to appear if the animals 
are curarized or if artificial respiration is practised. Funder's 
investigations indicate that reflex rather than purely mechanical 
causes are responsible for the symptoms (see page 41). Burton- 
Opitz has shown that distention of the intestine alone may cause 
a great diminution of the blood-flow in the mesenteric vessels 3 (see 
pp. 183 and 306). 

Renal and Biliary Colic. — Attacks of renal and biliary colic may 
be associated with marked increase in arterial pressure, a phe- 
nomenon which, while partly due to pain, is probably the result of 
reflex vasomotor constriction. This sudden increase of tension 
may account for the production of cardiac murmurs which have 
been reported as occasionally coincident with such attacks. 4 

Cerebral Vascular Crises. — The nervous phenomena of hypertension 
include headache, vertigo, convulsive seizures, paralyses (mono- 
plegia, hemiplegia), aphasia, dementia, etc. These symptoms may 
occur spontaneously and after lasting for a few hours disappear 
almost as suddenly as they appeared. The generally accepted belief 

1 Schlesinger, Deut. med. Woch., August 22, 1912, No. 34, p. 1592. 

2 Meteorismuss u. Kreislauf, Mitt. u. d. Grenz. d. Med. u. Cbir., xv. 3 and 4. 

3 Burton-Opitz, R., Ueber d. Stromung des Blutes in dem Gcbiete d. Pfortader, 
Arch. f. d. ges. Physiol., 1908. cxiv, 479. 

' Riesman, D., Cardiac Murmurs during Attacks of Biliary Colic, Anier. Jour. 
Med. Sci., November, 1911. 



VASCULAR CRISES 261 

at present is that they are due, as was first suggested by George 
Peabody, 1 to local vascular spasm. Organic lesions, hemorrhages 
or edema may perhaps also produce only transient effects, but the 
duration in such cases is longer and the recovery more gradual. 
Intermittent closing and opening of the cerebral vessels is by far 
the most tenable hypothesis upon which to explain brief, temporary 
attacks of paralysis. Sir William Osier, 2 who has recently reported 
two Aery dramatic cases, states that temporary aphasia is one of 
the commonest of these transient manifestations. '■' Inability to 
talk, the consciousness of it, no paralysis, emotional disturbance 
and, within a few hours, complete recovery," are characteristics. 
As high as twenty such attacks may occur before the patient 
succumbs to some of the eventualities of arteriosclerosis. With the 
disappearance of symptoms the pressure falls (often 30 to 50 mm.) 
to the patient's normal level. 

Vertigo is, according to Finkelnberg's 3 investigations, generally 
associated with an increase of the minimum pressure and a decrease 
of the blood-pressure quotient. This diminution of pulse volume 
which is often associated with pallor, weakness, and syncope 
apparently results from cerebral anemia. Vertigo may occur in 
either high or low tension cases as a result of cerebral anemia. It 
has been suggested that rotary vertigo of labrynthine origin always 
results from bilaterally unequal vasomotor influences along some 
portion of the coordinating tracts. 4 

Apoplexy. — Vascular rupture is naturally more apt to occur if 
blood-pressure changes in addition to being great are sudden. 
The marked pressure effects of violent muscular action, especially 
when associated with volitional effort or psychic stimulation have 
been alluded to. It is not surprising, therefore, to find that fits 
of anger, fright, sudden stooping or heavy lifting, especially after 
a full meal, straining at stool, coitus, etc., are often the precipitating 
causes of vascular rupture and anginal attacks. The history of a 
preceding transient hemiplegic attack is not infrequently obtained 
in cases that ultimately succumb to apoplexy (see Hemiplegia). 

Peripheral Vascular Crises. — This group includes intermittent 
claudication, erythromelalgia, and Raynaud's disease. In each 

1 Trans. Assoc. Amer. Phys., 1891, vi, 170. 

2 Transient Attacks of Aphasia and Paralysis in States of High Blood-pressure 
and Arteriosclerosis, Canadian Med. Assn. Jour., October, 1911. 

3 Ueber Blutdruckmessung bei Serrwindel, Miinch. med. Woch., 1906, hi, 238. 

4 Fowler, E. P., The Origin of Labrynthine Rest-tone, Jour. Am. Med. Assn., 
1915, lxiv, 118. 



262 BLOOD-PRESSURE IN ARTERIOSCLEROSIS 

case there is believed to be a disturbed balance between the vaso- 
dilator and the vasoconstrictor nerves. 

There is reason for believing that some of these cases owe their 
origin to an undue excitability or exhaustion of the sympathetic 
nervous system. In a case reported by Zweig 1 there were acute 
hallucinations, recurring urticaria, and sudden symptoms of hyper- 
thyroidism. These symptoms bore no direct relation to each other 
but were all, it seemed, different expressions of sympathetic lability, 
due perhaps to some abnormality of the internal secretions, thus 
differing from the true exophthalmic goitre cases in which the 
thyroid syndrome is primary. The results of studies in this class 
of cases reported by different investigators have been quite variable. 
Curschmann 2 found that psychic and thermic stimuli failed to 
produce plethysmography reactions. Stewart 3 found that the 
application of cold was followed by an increased instead of a 
diminished flow; and Simons 4 has reported great variability and 
asymmetry of vascular response. In Raynaud's disease it is believed 
that the arterioles are so contracted that blood-flow is practically 
occluded. Experimental evidence proves that this is quite possible. 
Macwilliam and Kesson 5 have shown that an occlusive spasm 
capable of resisting a pressure of 440 mm. Hg. may occur in diseased 
arteries as large as the metacarpal and metatarsal of the horse. 
Balaauw 6 has commented on the fact that spasm of the retinal 
vessels in cases of Raynaud's disease has probably never been 
authentically reported. 

II. Angioneurotic Manifestations. — Abnormal vascular responses 
to stimuli produce a number of different symptoms which have 
been designated by Cohen as vasomotor ataxia. To this group 
belong dermographism, urticaria, angioneurotic edema, chilblains, etc. 
A patient studied by Hewlett 7 who had dermographism and chil- 
blains reacted to the local application of moderate cold (which 
precipitated his symptoms) by a definitely increased blood-flow in 
the arm exposed in comparison to its fellow. The normal reaction 

1 Zur Kasuistik u. Aetiologie vasomotorischtrophischer Storungen, Berlin, klin. 
Woch., 1912, xlix, 2268. 

2 Untersuchungen ueber d. funktionelle Verhalten d. Gefasse bei tropischen u. 
vasomotorischen Neurosen, Munch, med. Woch., 1907, liv, 2519. 

3 The Measurement of Blood-flow in the Hands, Heart. 1911. iii, 33. 

4 Plethysphygmographische Untersuchungen d. Gefassreflexe bei Xervenkranken, 
Arch. f. Anat. u. Physiol. Phys., Abteil. 1910, Supplement, Band ccccxxix. 

6 Heart, 1913, iv, 298. 

6 Die Augen-symptome d. Raynaudschen Krankheit, Augenheilk., 1913. ix. Heft 5. 

7 Active Hyperemia following Local Exposure to Cold, Arch. Int. Med., 1913, 
xi, 507. 



VASCULAR CRISES 263 

to cold is of course just the reverse of this. The exudation may be 
serous or sanguineous, but in either case a marked local vasomotor 
disturbance exists. Osier has suggested that this group of ailments 
are all due to different degrees of the same poison. The abdominal 
crises of angioneurotic edema and purpura, a number of which 
have been attacked by the surgeons as a result of a mistaken 
diagnosis, have shown only local visceral edema or hemorrhage. 

Abnormal local vasomotor phenomena are also exemplified by 
(1) the tdche cerebrate — a red line with white margins, produced 
by irritating the skin by drawing the finger nail across it. This is 
seen in meningitis, typhoid fever, etc. (2) The white line of adrenal 
insufficiency; a localized blanching of the abdominal skin produced 
by means of the finger nail, seen in Addison's disease and other 
conditions associated with low blood-pressure. It is directly due 
to local reflex capillary spasm. Neither of these two conditions 
is constant nor diagnostically of much importance. 

Vascular Crises in Children. — While vascular crises are chiefly 
seen in arteriosclerotic individuals, angiospastic manifestations 
have also been described in children. Thus Kirsch 1 has reported 
attacks of localized gastric pain, associated with a heaving cardiac 
impulse, tortuous carotids, and a tense and pulsating abdominal 
aorta, which he attributes to vascular spasm. Hamburger also 
calls attention to certain subjective symptoms relating to the heart, 
and to objective vascular manifestations due to this cause. 2 

Under the former are found palpitation, unpleasant sensations 
in the precordium, such as a "stitch," and a feeling of oppression. 
Palpitation occurs after physical exertion and to a less degree after 
psychical disturbances. In marked cases more or less pain and 
dyspnea may occur, and even symptoms comparable to the 
angina pectoris of adult life. These symptoms are, however, rare 
in comparison to palpitation. Objectively there is found a heaving 
somewhat diffused apex beat, and slight epigastric pulsation. The 
boundaries of the heart are normal, or but slightly increased ; 
the sounds are clear. The epigastric pulsation is, in Hamburger's 
opinion, due to the descending aorta and not to the right ventricle. 
The lability of the pulse is shown, on the one hand, by a rapid 
increase in the rate on sitting up, standing, and on slight physical 
exertion ; and on the other hand, by a pulsus irregularis respiratorius, 

1 Gefiisskrisen im Kindesalter, Mitteil. d. Gesellsch. f. inn. Med. u. Kinderheilk., 
Wien, 1912, ii. S. 190-194. 

2 Munch., med. Woch., 1911, lviii, 2201. 



264 BLOOD-PRESSURE IN ARTERIOSCLEROSIS 

increasing with inspiration and diminishing with expiration. This 
symptom is most marked in severe cases, but also occurs in normal 
children. Among the subjective circulatory symptoms are headache, 
similar in onset to migraine, but involving both sides of the head, 
usually in the occipital region. Sudden local anemias of the brain 
cause dizziness and unconsciousness, these symptoms and the head- 
ache being due not to a general anemia, as is often supposed, but 
to changes in the vasomotor system. A tendency to cold hands and 
feet is another symptom of this class, and also the above-mentioned 
cardiac pains due, according to Nothnagel, to an ischemia of the 
heart muscle. Among the objective circulatory signs are noted flush- 
ing or paling on psychical disturbance, coldness of the extremities, 
dermographia, visible pulsation of the carotids, and increased 
tension of the arterial walls in the radial and temporal arteries. 
Certain forms of bronchial asthma probably belong to this class. 
There are, besides, a large number of symptoms occurring in com- 
bination, all of which can be traced back to a nervous irritability 
of the whole circulatory apparatus. This "vasoneurosis" is by 
far the most prominent and important manifestation of nervousness 
in later childhood (seven to fourteen years), and occurs also in 
younger children. 

The rigidity of the arterial walls in nervousness is marked in 
many cases, and generally all children with apparently "thick- 
ened" arteries are nervous. Normally, under six years, the pulse 
only, and not the arterial wall, is felt by the fingers; and not until 
the tenth year are the arterial walls frequently palpable. Pallor, 
especially in school children, is often construed to be an anemia, 
whereas it is arterial contraction due to nervousness; such children 
commonly have dark rings under the eyes. Marked vasoneurotic 
symptoms do not usually begin until about the seventh year, 
when the child begins to attend school. As etiological factors 
Hamburger attributes an inherited disposition and certain psychical 
and physical irritating or stimulating influences, such as fright and 
joy and autosuggestion on the one hand, and toxins on the other. 
The prognosis of the vasoneurotic condition is good if psychical 
causes can be discovered and avoided, and the child's disposition 
modified by good hygiene and intelligent mental training. 

A number of the symptoms and signs which Hamburger describes 
are also met with in constitutionally hypotensive individuals. 

The Treatment of Peripheral Arterial Spasm. — Cramps in the 
Legs. — Nocturnal cramps in the lower extremities are of common 



VASCULAR CRISES 265 

occurrence in hypertensive disease. The patient is often suddenly 
aroused from his sleep by an intense, muscular cramp of great 
severity. These cramps, which are a result of vasomotor spasm 
may sometimes be relieved by tightly tying a string, tape or hand- 
kerchief around the extremity above the point of pain, or by rubbing 
the limb vigorously with stiff brushes. The inhalation of amyl 
nitrite has in my experience not been very satisfactory, and im- 
mersion of the extremity in hot water is usually not feasible because 
the cramp is generally over before the water can be obtained. As 
a remedy for chilblains, Raynaud's disease and other conditions 
due to vasomotor ataxia, Brunton advises the use of the salicylates 
either with or without the bromides. He has also seen good results 
follow the administration of thyroid extract in small doses. (See 
Treatment of Animal Hypertension, p. 299.) 



CHAPTER XII. 

ARTERIAL HYPERTENSIVE CARDIOVASCULAR 
DISEASE, NEPHRITIS, Etc. 

Blood-pressure variations of from 10 to 30 mm. Hg., and 
perhaps more, may be purely physiologic in their nature. We can 
draw conclusions of the import of pressure variations only if they 
exceed these amounts, or if they are more or less regularly encoun- 
tered in the same individual. A systolic pressure constantly above 
160 mm., or a diastolic pressure constantly above 100 mm. Hg., 
is definitely pathologic al any age. The younger the subject with 
such a pressure the more abnormal must it be considered. Before 
middle life 145 mm. should not be exceeded. 

Arterial sclerosis is often very variable in its distribution. As 
an example, the tendency for syphilis to involve the ascending 
aorta may be mentioned. Extreme degrees of nodular peripheral 
sclerosis often occur without corresponding involvement of the 
splanchnic vessels, and, on the other hand, severe renal vascular 
lesions may be associated with only moderate peripheral thickening. 
Palpation of the radial artery is therefore not a procedure by which 
we can estimate the seriousness of arterial degeneration, nor is 
the absence of an accentuated aortic second sound — although this 
is usually present — an indication that arterial pressure is not 
increased. The view that peripheral arteriosclerosis and cardiac 
hypertrophy are secondary to hypertension is constantly receiving 
corroboration. It is therefore quite erroneous to speak of "hard- 
ening of the arteries" as the cause of increased blood-pressure, 
since it is the latter which is the cause of the former. 

The height of the diastolic pressure is often more important than 
that of the systolic tension. The former is far less subject to 
temporary variation and it further indicates the resistance which 
the heart has to overcome. It is also more of an index of the mean 
pressure than is the systolic pressure. A constant diastolic pressure 
of or above 100 mm. indicates hypertension regardless of whether 
the systolic pressure be 180 or 140 mm. 



THE SIGNIFICANCE OF HYPERTENSION 207 

THE CARDIAC OVERLOAD IN HYPERTENSION. 

Under normal conditions we often find the systolic pressure 
about 120, the diastolic pressure about 80, the pulse pressure, 
therefore, 40. "Thus the amount of energy expended in maintain- 
ing the circulation in excess of that required to open the aortic- 
valves and overcome the resisting pressure of 80, is 40. The normal 
load may therefore be considered -f f , or 50 per cent, of the diastolic 
pressure" (Stone 1 ). Applying this conception to hypertension 
it is apparent that a systolic and diastolic pressure of 170 and 
100 mm. respectively yielding a pulse pressure of 70 would furnish 
a heart load of tVo" (70 per cent.), or an overload of 20 per cent. 
Stone's studies indicate that while the clinical symptoms of hyper- 
tension generally do not appear until the overload exceeds 25 per 
cent., and while with a modification of the habits of life 50 per cent, 
may be borne, yet with an overload of 50 per cent, myocardial 
exhaustion may be precipitated by any sudden strain. We have not 
found the pulse pressure percentage of the diastolic pressure, 
"the cardiac load," of any value in the estimation of circulatory 
efficiency. 

THE SIGNIFICANCE OF HYPERTENSION. 

Given a patient with a well-marked hypertension (190 mm. 
systolic and 110 mm. diastolic) we are de facto warranted in assuming 
that the patient is suffering from Bright's disease, at least until 
further investigation has shown that the hypertension is due to 
some other cause. Authenticated cases, substantiated by autopsies, 
are on record in which the kidneys of such cases have been entirely 
normal, but such instances are the exception. 2 To what the rise of 
pressure in such cases is due has not been satisfactorily explained, 
but arteriosclerosis alone without some renal involvement rarely, 
if ever, produces hypertension. The absence of albumin and casts 
does not necessarily exclude disease of the kidneys; furthermore, 
repeated and careful urine examinations will often show character- 
istic findings in cases which, on a few examinations, may yield 
negative results. It is of vital importance that nephritic changes 
be discovered early, and therefore an arterial pressure disproportion- 

1 The Clinical Significance of High and Low Pulse Pressures with Special Refer- 
ence to Cardiac Load and Overload, Jour. Amer. Med. Assoc, 1913, lxi, 1256. 

2 Krehl, Ueber die krankhafte Erhohung des arteriellen Druckes, Deut. med. 
Woch., 1905, xxxi, 1872; Schlayer, Untersuchungen ueber d. Funktion kranken 
Nieren, Deut. Arch. f. klin. Med., 1911, cii, 371. 



268 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

ately high in relation to the age of the individual always calls for 
careful investigation, not only by means of the routine urine 
examinations but also, if possible, by some of the functional renal 
tests, preferably phenolsulphonephthalein. It should be remembered 
that in the early stages increased blood-pressure may be only 
intermittently present. The normal physiologic causes which raise 
arterial tension in nephritic cases produce an exaggerated response. 
In the later stages of the disease, when the cardiovascular system 
is weakening, the pressure often falls, but such a fall is generally 
coincident with the appearance of untoward symptoms and physical 
signs — dyspnea, vertigo, palpitation, a diminished urinary output 
edema, etc. These occurrences may also be brought about if a 
high pressure be forcibly reduced by means of the nitrites; indeed, 
uremia may thus be precipitated. 

No definite general rules can be laid down for the prognostic 
or therapeutic import of a fall or a rise of blood-pressure. The 
significance of such an event depends both on the nature of the 
disease and on the state of the patient. In patients seriously ill 
a rise may indicate improvement, whereas the same finding in a 
case of arteriosclerosis or nephritis may mean that uremic mani- 
festations are impending. Again, in the case of cardiovascular 
disease, increase of pressure may' indicate better compensation and 
elimination and be associated with general improvement. A fall 
of pressure, however, may also be a harbinger of good omen as 
indicating a lessening of toxic products and carbon dioxid accumu- 
lation, and peripheral vasoconstriction — the class of case which 
Sahli has described as "high-pressure stasis." The fall of pressure 
just alluded to may be merely a fall of the systolic pressure or 
such a fall associated with an increase of the pulse pressure, which, 
were it always demonstrable, would afford an easily comprehensible 
explanation of the physical improvement. Such is, however, by 
no means always the case. Some cases show marked improvement 
coincident with a decrease of both maximum and pulse pressure. 
Capillary pressure, upon which nutrition depends, does not vary 
directly with arterial pressure, but is rather dependent upon the 
state of the arterioles and the veins. High pressure is not neces- 
sarily associated with a good, nor low pressure with a poor, circula- 
tion in the capillaries. If the arterioles are contracted the arterial 
pressure, however high, fails to reach the capillaries. 

Classification of Arterial Hypertension. — A satisfactory classifica- 
tion of the cases of arterial hypertension cannot be made until our 



THE SIGNIFICANCE OF HYPERTENSION 209 

knowledge of the etiologic factors is more complete, hut certain 
types are more or less well differentiated. Arterial hypertension is 
met with in association with: 

1. Demonstrable nephritis, as evidenced by urinary findings, 
retinal lesions, cardiac hypertrophy and accentuation of the aortic- 
second sound. 

2. Demonstrable arteriosclerosis as indicated by radial thickening 
(leathery arteries), tortuosity of the temporal arteries, cardiac- 
hypertrophy, retinal arteriosclerosis (front-piece). Syphilis is the 
common cause of this type. 

3. A combined type in which both renal and arterial lesions are 
manifest. 

4. Non-nephritic hypertension (essential hypertension). — Regard- 
ing this variety of the disease, if the hypertension of polycythemia is 
excluded, there is great difference of opinion. 

Some authorities hold that latent glomerulonephritis is the cause 
of the increased blood-pressure; others maintain that it is a distinct 
pathologic entity due to some as yet unknown and probably chemi- 
cal cause, such as auto-intoxication or abnormality of endocrine • 
secretion. 

Riesman 1 whose classification has just been given, emphasizes 
the importance of recognizing a variety of non-nephritic hyper- 
tension occurring often in women past middle life, who are obese, 
undersized, ruddy complexioned and possessed of considerable men- 
tal and physical energy, without demonstrable arterial or renal 
abnormalities. The men of this group are apt to be deep-chested, 
robust and great expendors of energy. Obesity is per se not in- 
frequently associated with arterial hypertension. Among 59 cases 
without apparent renal or vascular disease, 16 showed pressures 
between 145 and 160 mm., 9 between 165 and 180, and 4 between 
185 and 250 mm. Hg. 2 

This class represents a large and important group of hypertension 
cases but many of them die a nephritic death, although this may not 
occur for many years after the onset of the increased pressure. 
The writer is of the opinion that many of these cases are due to a 
latent nephritis, but that certainly all of them are not. In the 
essential hypertension cases the blood-pressure is generally lower 
in both its phases than in the nephritic group. It is also more 

'Are We Exaggerating the Dangers of Arterial Hypertension? Penn. Med. 
Jour., December, 1914. 

2 Faber, Ugeskrift f. Laeger., 1915, lxxvii, No. 23. 



270 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

amenable to treatment. As a rule the dietetic treatment of these 
cases may be much more liberal than in the nephritic group. 

The Symptoms of Arterial Hypertension. — Cardiovascular Symp- 
toms. — Dyspnea, palpitation, vertigo, oppression — often on going 
to bed — cardiac erythism, angina pectoris, muscular cramps, spon- 
taneous or on exertion, edema of lungs, arhythmia. 

Renal Symptoms. — Polyuria, with nocturnal micturition — the 
urine having a low specific gravity and containing a few hyaline 
or granular casts and a trace of albumin. 

G astro-intestinal Symptoms. — Dyspeptic manifestations with 
eructations, flatulence, postprandial discomfort, hyperacidity, 
constipation, epigastric pain, tenderness, or oppression. 

Nervous Symptoms. — Matutinal headache, nervousness, restless- 
ness, irritability, inability to concentrate, easy fatigue from mental 
exertion, insomnia, numbness, tingling, migraine, transitory aphasia, 
hemiplegia, apoplexy. 

Ocular Symptoms. — (a) Spasmodic symptoms, without definite 
anatomical lesions: amblyopia, transient amaurosis, hemianopia. 

(6) Constant symptoms, with increased pressure of cerebrospinal 
and cerebro-arachnoid fluid. They tend to be progressive and 
may lead to subconjunctival or retinal hemorrhages, glaucoma, 
etc. (see page 407). 

Aural Symptoms. — Tinnitus aurium, either with or without 
vertigo. (See page 261). 

It frequently happens that the subjects of arterial hypertension 
complain only of respiratory or gastrointestinal symptoms. Unless 
blood-pressure elevation and cardiac hypertrophy are sought for 
by the examiner the true etiological factor is apt to be overlooked. 
Indigestion, bloating after meals, slight dyspnea on exertion, and 
nocturnal micturition are very suggestive manifestations. Such 
individuals are usually overweight — overfed and underexercised — 
especially in the case of men who have a plethoric, robust appear- 
ance. But hypertension also occurs in abstemious individuals, and 
in such seems to bear a very frequent relation to overwork, worry, 
and insufficient relaxation. According to Yolhard, 1 the Japanese 
are rarely the subjects of arterial hypertension, a fact which suggests 
that diet and mode of life may account for their relative immunity. 
Severe or recurrent epi.sta.ris is sometimes associated with and due 
to arterial hypertension and in such cases may act beneficially in 
reducing the pressure. 

1 Ueber d. funktionelle Unterscheidung der Schrunipfnieren. Kong. f. inn. Med. 
xxviii, 735. 



THE SIGNIFICANCE OF HYPERTENSION 271 

Physical Signs. — Heart. — Hypertrophy — chiefly left-sided, accen- 
tuation, splitting or reduplication of the aortic second sound; later, 
systolic murmurs at the mitral or aortic areas are often found. 
Cardiac or aortic dilatation, arhythmia — generally extrasystolic — 
or when compensation fails, auricular fibrillation; bradycardia, 
rarely pulsus alternans. 

Arteries. — Flushing and duskiness of the face and hands; a hard, 
relatively incompressible pulse. Cervical pulsation, prominent 
and tortuous superficial arteries (temporal, brachial), arterial 
sounds. Retinal vascular sclerosis, rhythmic movements of the 
head (pulsatile), arcus senilis. 

In most of the cases high blood-pressure is mainly the result 
of vascular spasm. Thus there may be, for example, relatively 
normal bloodvessels with marked vascular contraction, or distinct 
fibroid changes with moderate spasm. Marked lability of blood- 
pressure is common. We have seen that in health pressure varia- 
tions are constantly brought about by diverse influences. In 
arterial hypertension all such responses are exaggerated, and 
although arteriolar pressure is high, capillary pressure is low. 
Intercurrent infections generally cause a temporary fall of pressure. 
When high pressure has been long standing we frequently find a loss 
of vascular compensation which results in a lowering of pressure, 
simply because the arterial musculature is no longer able to maintain 
a high degree of tonicity. The arteries become relaxed, tortuous, 
stretched, and are prominent on inspection. Such a break in vascular 
compensation may temporarily give relief to an overburdened heart, 
but usually does so at the cost of general nutrition and sometimes 
precedes a progressively downward course from insufficient renal 
activity. Such a broken cardiovascular compensation accounts 
for the secondary fall of pressure often seen in the late stages of 
arteriosclerosis. 

The exact mechanism which leads to dilatation of the arteries is still 
uncertain. The transplantation of sections of a vein into an artery, 
after the method of Carrel, does not lead to a dilatation of the 
vein, despite the greater pressure to which it is, in its new situation, 
exposed; in fact, a thickening and decrease in caliber results. 
This fact would indicate that "increased blood-pressure cannot in 
itself produce a lasting progressive dilatation of the bloodvessel." 1 

Moderate pressures are naturally better borne than very high 

1 Fischer and Schmieden, Frankfurt Zeitsch. f. Path., 1909, iii. s. 



272 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

ones, and as a general rule ambulant patients with constant pressures 
of 170 mm. are in no immediate danger. A systolic tension of 200 
mm. and over, however, renders sudden catastrophies not unlikely, 
although such cardiovascular strains may be borne for eight or 
ten years (see p. 131). 

Arterial hypertension is more common in men than in women, 
but high pressures are generally better and longer endured by the 
latter, owing to their more ready adaptability to a restricted life 
and to their lessened exposure to sudden hypertensive influences. 

In some cases of hypertension marked slowing of the pulse is a 
striking clinical feature which, in the absence of local cardiac 
disease of the conductive system, is due to the fact that hypertension 
stimulates the cardio-inhibitory centre. This inhibitory action is 
brought about either by the direct effect of increased pressure 
in the vessels supplying the cardio-inhibitory nerves, or reflexly 
by stimulation of the peripheral nerves in the vessels. Increased 
pressure in the left ventricle has little effect, but in the thoracic 
aorta the effect is more marked. This reflex stimulation may 
disappear while the effect of direct pressure on the bloodvessels 
of the cardio-inhibitory centre still remains. 1 

NEPHRITIC HYPERTENSION. 

The increased blood-pressure which occurs in connection with 
renal disease, especially with that form which is clinically designated 
as chronic interstitial nephritis, is the most striking and diag- 
nostically perhaps the most important abnormality of arterial 
tension which is met with in the entire domain of medicine. There 
seems to be a tendency to revert to the old concept of Gull and 
Sutton, that chronic interstitial nephritis results from general and 
not merely local disease of the arterioles — that it is primarily 
a vascular disease of which the renal changes are but secondary 
manifestations. Certainly it is a fact that the clinical pictures 
as well as the blood-pressure findings of chronic interstitial nephritis 
are quite different from those seen in the "parenchymatous" 
variety of renal disease. Whether the rise of blood-pressure occurs 
before structural vascular lesions exist is still in question. The belief 
that it does has been put forth by von Basch ("angiosclerosis"), 
by Huchard ("presclerosis"), and by Allbutt ("hyperpiesis"). 

1 Eyster and Hooker, Slowing of the Pulse from Increased Blood-pressure, Amer. 
Jour. Phys., 190S, xxi, 373. 



NEPU HI Tl ( ' II YPERTENSION 273 

Hyperpiesis. — The term hyperpiesis has been applied to hyper- 
tension not due to demonstrable renal, cardiac and arterial disease. 
It is suspected that if unchecked this condition may be an ante- 
cedent of organic hypertension. In arteriosclerotic conditions 
the increased blood-pressure, at least up to a certain point, sub- 
serves a necessary function; in hyperpiesis, so far as we can 
determine, the pressure increase in addition to being sudden and 
associated with unpleasant symptoms subserves, no useful 
function. 

Glomerulonephritis. — The recent studies of Volhard and Fahr 1 
have emphasized the fact that blood-pressure is increased in diffuse 
glomerulonephritis regardless whether the condition is acute, 
chronic or in its terminal stage, whereas simple degenerative 
nephritis (parenchymatous nephritis) — disease of the epithelial 
tubules — is not associated with hypertension. In the interval 
between the acute and the terminal stage of glomerulonephritis, 
increased blood-pressure, together with slight albuminuria and 
occasional casts are the only signs of Bright's disease, other renal 
tests showing normal results. 

Simple Renal Sclerosis. — The highest blood-pressures are often 
met with in renal arteriosclerosis, in cases in which the intima of 
the smallest renal arterioles is thickened and in which only occasional 
glomeruli or tubules show abnormalities. This condition has been 
termed simple or benign sclerosis, since it is compatible with many 
years of useful life. This type of renal disease corresponds to Gull 
and Sutton's primary vascular disease. Its close connection with 
the heart both in its symptomatology and mode of termination 
(cardiac failure) has led Janeway to suggest the term cardio- 
vascular hypertensive disease. Ten or fifteen per cent, of these 
cases, however, insidiously develop renal symptoms such as albumin- 
uric retinitis, decreased phthalein elimination, polyuria or increased 
non-protein or urea nitrogen in the blood. Such cases clinically 
and sometimes histologically represent a combination form of the 
simple sclerotic and the glomerulonephritic types. 

In this type of renal disease cardiac hypertrophy is marked, 
especially if the arterial changes in the kidney begin early in life. 
When developed later in life the frequently associated coronary 
sclerosis renders cardiac hypertrophy less readily possible. Among 



1 Die Brightische Nierenkrankheit, Berlin, 1914. For an excellent resume see 
Austin, J. H., Prog. Med., 1915. 
18 



274 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

268 cases studied by Volhard and Fahr, 102 had a systolic pressure 
above 200 mm.; 104, between 170 and 200 mm., and only 61 
pressures below 170 mm. 

Symptoms. — The symptoms of functional hypertension may 
be any of those seen in the organic variety. The pressure readings 
associated with such symptoms are characterized by their lability, 
the exacerbations of pressure being evidently spastic in origin. 
Hyperpiesis occurs in men after middle life, and in women at the 
time of the menopause (see page 396) . A disturbed balance between 
the organs of internal secretion, especially the thyroid, the adrenals 
and the sexual glands, has been suggested as a possible cause. 

In the vast majority of cases a systolic blood-pressure of over 
160 mm. and a diastolic pressure of over 100 mm., if constantly 
present, points indubitably to that symptom-complex which is 
designated as interstitial nephritis, especially if it be associated 
with polyuria and urinary abnormalities. It does not necessarily 
mean, of course, that the individual in question will die of uremia 
or dropsy, for many cases succumb to cardiac or vascular lesions. 
Occasionally cases are encountered in which practically normal 
kidneys are found at autopsy, but as a general rule the small red 
atrophic organ is found. Many forms of renal disease are associated 
• with a slightly increased blood-pressure, the notable exceptions 
being degenerative {tubular) nephritis, amyloid disease, suppurative 
pyelonephrosis, and tuberculosis. 

Arterial hypertension is generally a condition of gradual develop- 
ment extending over years of time, with a tendency to increase, 
and with periods of spontaneous intermission or exacerbation. 
These latter are often, but by no means always, traceable to hygienic 
or dietetic variations. They are very closely associated with 
psychic phenomena which are generally by far the most potent 
factors for good or ill. 

The degree of tension which can be borne without subjective 
consciousness is mainly an individual question, but a pressure of 
180 mm. is not often exceeded without symptoms, and constant 
pressures of 200 mm. or over are generally not long maintained 
before leading to some sudden catastrophe, such as angina pectoris, 
uremia, or apoplexy. The significance as well as the seriousness 
of high blood-pressure often receives useful elucidation as the 
result of an ophthalmoscopic examination. 

Etiology. — Volumes have been written based upon clinical and 
pathologic findings, upon theoretic considerations, and upon 



NEPHRITIC HYPERTENSION 275 

experimental evidence to account for nephritic hypertension, since 
1836, when Richard Bright 1 described the disease which now bears 
his name, and suggested as a cause of the cardiac hypertrophy 
which occurs in many cases, even in the absence of valvular disease: 
(1) "That the altered quality of the blood affords irregular and 
unwonted stimulus to the organ immediately," or (2) "that it 
so affects the minute and capillary circulation, as to render greater 
action necessary to force the blood through the distant subdivisions 
of the vascular system. ' ' 2 The subject, which cannot be exhaustively 
discussed here, has recently been most ably reviewed by Janeway, 
from whose article I have freely drawn. 3 

It is now generally believed that the cardiac hypertrophy is in 
nearly all cases due to arterial hypertension, and to explain the 
cause of the latter a number of hypotheses have been offered. 

I. Mechanical Theories. — The old mechanical theory of Traube, 
which attributed the hypertension to resistance in the kidney itself, 
and which had almost fallen into oblivion (since ligature of the 
renal vessels does not produce an increase of blood-pressure), has 
recently been rejuvenated. Katzenstein has reported that in a 
dog constriction of the renal arteries, without complete obliteration, 
leads to an increased pressure. These results were not corroborated 
by others. Thus Alwens, 4 by placing the kidneys in an oncometer 
without touching the vessels, on increasing the pressure 2 or 3 mm. 
Hg. above the arterial tension, found that blood-pressure in the 
aorta rose and was maintained as long as renal compression con- 
tinued. But in these experiments the flow from the renal vein 
was diminished, almost suppressed, a fact which renders the experi- 
ment incomparable to nephritis, in which no such obstruction to 
venous outflow exists. Embolization of the kidney with paraffin, 
as practised by Miiller and Maas, did not increase blood-pressure. 
The blood flowing through the kidneys under normal and under 
increased pressure generally shows no increase in flow, "even at the 

1 Jores found that the absence of hypertrophy in advanced interstitial nephritis 
is usual in the form known as the secondary contracted kidney. In the typical red 
granular kidney hypertrophy is the rule, with, however, occasional exceptions. 
Verhandl. d. deutsch. path. Gesellsch., 1908, xii, 187. 

2 Bright, R., Cases and Observations Illustrative of Renal Disease Accompanied 
with the Secretion of Albuminous Urine, Guy's Hospital Reports, London, 1836, i, 
338. 

3 Janeway, T. C, Nephritic Hypertension, Clinical and Experimental Studies, 
Aroer. Jour. Med. Sci., 1913, cxlv, 625 (bibliography). 

4 Experimentelle Untersuchungen u. d. Bedeutung d. mechanischen Theorie d. 
nephritischen Blutdrucksteigerung, Deut. Arch. f. klin. Med., 1909, xcviii, Nos. 2 
and 3. 



276 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

time when very pronounced rises in arterial pressure had developed" 
(Burton-Opitz and Lucas). 1 

Loeb 2 demonstrated the fact that the degree of arterial hyper- 
tension bore a more or less definite relation to the degree of glo- 
merular renal involvement, and suggested that the increased pressure 
was a reflex compensatory effort of the system — an attempt to 
supply, by means of splanchnic constriction, an adequate blood- 
supply which local vasodilatation alone was no longer capable of 
furnishing. This attractive hypothesis has, however, been proved 
incorrect by Jores and others, who have shown that glomerular 
changes were often conspicuously slight when blood-pressure was 
highest, and vice versa. Furthermore, as has been recognized by 
many, and recently emphasized by Janeway, "amyloid disease, 
which is par excellence a disease of the glomeruli, in its pure form 
is almost invariably without effect on the blood-pressure, and 
without an accompanying hypertrophy of the heart. This fact 
is one of the most difficult to be reconciled with any theory of 
nephritic hypertension . ' ' 

II. Chemical Theories. — The chemical hypothesis attributes the 
increased blood-pressure to substances in the blood as resulting 
from either (1) insufficient renal elimination; (2) disturbances of 
internal secretion; (3) toxic substances set free by the diseased 
kidney. 

Following the suggestion of Bright, that an altered composition 
of the blood might account for the cardiovascular changes, it was 
for a time believed that hypertension was due to retained toxic 
products which the kidneys failed to eliminate, which produced first 
spastic hypertension and later arteriolar hypertrophy. 

If after removing one kidney from a dog, portions of the remain- 
ing kidney (not exceeding two-thirds of the total kidney substance) 
be resected, the animals after developing polyuria ultimately die 
of cachexia. Five among eighteen dogs upon whom these graduated 
nephrectomies were practised by Paessler and Heineke 3 showed 
an average blood-pressure increase of 21.5 mm., together with 
left ventricular hypertrophy. They found that after destruction 
of a certain amount of kidney substance the quantity of urine 
increased, but was poor in extractive substances, especially the 

JJour. Exp. Med., 1911, xiii, 308. 

2 Ueber d. Blutdruck u. Herzhypertrophie bei Nephritikern, Deutsch. Arch. f. 
klin. Med., 1905, lxxxv, 348. 

3 Versuehe z. Pathologie d. Morbus Brightii, Verhandl. d. deutsch. path. Gesellsch., 
1905, ix, 99. 



NEPHRITIC HYPERTENSION 277 

nitrogenous elements which tended to accumulate in the blood 
and the tissues. The same phenomena perhaps occur in nephritis, 
but they do not manifest themselves for a long time. There is a 
polyuria at the beginning; later extractive substances are eliminated 
in diminished quantity; finally, nitrogen accumulation occurs in 
the blood and tissues, forming what is designated as the products 
of nitrogen retention. 

In a recent summary Paessler states that (a) cardiac hyper- 
trophy in nephritis is due to the renal disease; (b) as a result of 
the latter there occurs an increased stimulability of the vasocon- 
strictors causing spastic contraction of the arterioles; (c) that 
right-sided cardiac hypertrophy is secondary to left ventricular 
failure. These graduated nephrectomy experiments leading first 
to hypertension, polyuria, and albuminuria, and later to gastro- 
intestinal disturbances, cachexia, hypotension, and death, have 
been corroborated by Pearce 1 and Janeway. 2 The exact mechanism 
by virtue of which this hypertension is produced is still uncertain, 
but it is in all probability due to increased arterial tonus. It has 
been found experimentally that in gradually nephrectomized 
animals, arterial spasm is brought about by stimuli which in normal 
animals are insufficient to engender similar results. It must be 
borne in mind, however, that "although the results of reduction 
experiments are striking, the procedures by which they are obtained 
are not such as to involve only a single factor, but bring several 
forms of kidney injury into play; that is, reduction of functional 
substance and productive atrophic and vascular changes, accom- 
panied by the elimination of albumin and casts" (Pearce). 

Ten cases of high-grade hypertension were studied at autopsy 
by Herxheimer. 3 In no case was the parenchyma of the kidney 
microscopically normal, but in most cases the changes were small 
in comparison with the constant high-grade arteriosclerotic vascular 
degenerations, especially of the arterioles. In all ten cases extensive 
hyaline thickening and fatty degeneration of the intima occurred. 
Slight or complete obliteration of the lumen was found. In some 
cases especially the vasa afferentia of the glomeruli were involved, 

1 The Influences of the Reduction of Kidney Substance upon Nitrogenous Metab- 
olism, Jour. Exp. Med., 1908, x, 632; A Study of Experimental Reduction of Kidney 
Tissue with Special Reference to the Changes in that Remaining, Ibid., 1908, x, 745. 

2 Note on the Blood-pressure Changes Following Reduction of the Renal Arterial 
Circulation, Proc. Soc. Exp. Biol, and Med., 1909, vi, 109. 

3 Niere und Hypertonie, Verhandl. d. deutsch. path. Gesellsch., 1912, xv, S. 211- 
216. 



278 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

and also some loops of the glomeruli showed the fatty and hyaline 
degeneration. In addition, atrophy of the tubules, increase of 
connective tissue, infiltration of round cells were noted (the vascular 
changes of the old Gull and Sutton arteriofibrosis) ; in the other 
organs, in opposition to Jores's findings, there were only occasional 
vascular changes (in the pancreas, testicles, liver, and always much 
less extensive than in the kidney) . Only in the spleen were vascular 
changes constantly found, but among 410 spleens examined there 
was in 170 marked hyaline change in the intima of the small vessels, 
even in young people, so that the findings in the spleen have no 
particular weight. 

It seems, therefore, that although general arteriosclerotic changes 
occur, they are more marked in the kidneys than elsewhere, and that 
the arterial changes are the cause, not the result, of the arterial hyper- 
tension. 

Renin. — Retention of ordinary metabolites, such as urea, does 
not explain arterial hypertension, and many attempts have been 
made to identify pressor substances in the blood. Tigerstedt 
and Bergmann succeeded in extracting from a rabbit's kidney a 
substance (renin) which experimentally increased arterial tension 
when injected into animals. It has been suggested that autolysis 
of the diseased kidney causes this substance to be thrown off 
into the general circulation. 1 Ascoli found that nephrotoxic 
serum possessed hypertensive properties, while Riva-Rocci and 
Maragliano obtained a similar substance in increased quantity 
in the diseased kidney. While those findings have been widely 
quoted, Pearce 2 has definitely shown that nephrotoxins are not 
truly specific, that "the production of autonephrolysin by injuring 
one kidney was doubtful, and that Ascoli's claim of a blood-pressure 
raising substance could not be confirmed." 

Pearce 3 has shown experimentally that a dog's kidney, unlike 
that of a rabbit and certain other animals, does not contain a 
depressor substance. Of course it does not follow that the results in 
human nephritis run parallel with those of experimental nephritis, 
but a comparison is, to say the least, interesting. 

1 Shaw, H. B., Auto-intoxication; its Relation to Certain Disturbances of Blood- 
pressure, Goulstonian Lectures, Lancet, 1906, i, 1295, 1375, 1455. 

2 The Theory of Chemical Correlation as Applied to the Pathology of the Kidney, 
Arch. Int. Med., August, 1908. 

3 An Experimental Study of the Influence of Kidney Extracts and of the Serum 
of Animals with Renal Lesion on the Blood-pressure, Jour. Exp. Med., 1909, xl, 430; 
The Influence of Kidney Extracts on Blood-pressure, Arch. Int. Med., 1912. 



NEPHRITIC HYPERTENSION 279 

Moreover, the injection not only of saline kidney extract but 
also that of other organs except the adrenal, pituitary, and spleen, 
has failed to increase blood-pressure, 1 and last, although by no 
means least, "hypertension is most extreme in those intensely 
chronic types of nephritis in which breaking down of kidney sub- 
stance must be at a minimum if there is any at all" (Janeway). 

Epinephrin. — Although first suggested by Neusser, the hypothesis 
that nephritic hypertension is due to increased activity of the 
suprarenal glands was prominently brought to the fore by Vaquez 2 
and the main exponents of this doctrine are still to be found in 
France. 

Marcuse believes that as the result of the resistance thus opposed 
by the kidneys to the circulation, an enlargement of the inferior 
suprarenal artery, a branch of the renal artery, occurs. The supra- 
renal gland being thus oversupplied with blood secretes an increased 
quantity of epinephrin. The objection to this explanation lies 
in the fact that the inferior suprarenal artery is often lacking or, 
when present, is not given off from the renal artery. 

From an experimental standpoint it seems well established that 
there exists a definite physiologic antagonism between pancreas 
extract and adrenalin, regarding their effect on blood-pressure in 
normal animals. Zondek 3 has recently shown that pancreas extract 
exerts its usual hypotensive effects after the production of experi- 
mental nephritis. An injection of pancreas extract is capable of 
completely neutralizing increased blood-pressure in uranium and 
mercurial nephritis, but fails to do so in the case of chromium 
lesions. 

Although the epinephrinemia hypothesis is an attractive one, 
with certain facts to commend it, accumulating evidence points 
strongly to its fallaciousness. Thus it appears (1) that there is 
no constant relation between the degree or even the presence of 
hypertension and the anatomic structure of the glands. 4 (2) The 
results obtained by estimating the epinephrin content of the glands 
in different conditions are inconclusive. 6 (3) Most of the studies 

1 Miller, J. L. and E. M., The Effect on Blood-pressure of Organ Extracts, Jour. 
Physiol., 1911, xliii, 242. 

2 Hypertension, Proc. Congres Francaise de Med., 1904, p. 338. 

3 Beeinflussung des Blutdrucks d. akuten Experimentellen Nephritis d. Kannin- 
chens durch Pankreas extrakt, Deut. Arch. f. klin. Med., 1914, cxv, 1. 

4 Pearce, R. M., The Relation of Lesions of the Adrenal Gland to Chronic Nephritis 
and to Arteriosclerosis; an Anatomical Study, Jour. Exp. Med., 1908, x, 735; Bor- 
berg, Das Chromaffine Gewebe. Nebennierenuntersuchungen, Skand. Arch. f. 
Phys., 1912, xxviii, 91. (Abstr. Zentralbl. f. d. Ges. inn. Med., 1913, iv, 383.) 

5 Ingier and Schmorl, Ueber d. Adrenalingehalt. d. Nebennieren, Deutsch. Arch, 
f. klin. Med., 1911, civ, 262. 



280 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

based upon the adrenalin content of the blood are faulty because 
of lack of controls — in order to be conclusive the test should respond 
to a frog's eye, coronary artery, and intestinal ring method, and, 
as Janeway suggests, show not only qualitatively typical but also 
quantitatively possible epinephrin effects. (4) Recent physiologic 
evidence indicates that the adrenal glands are normally only 
intermittently active. They are emergency organs, but not con- 
stantly concerned with the maintenance of normal blood-pressure. 1 
All deductions based clinically or experimentally upon qualitative 
or quantitative analysis of adrenalin in the serum must be accepted 
with reserve. Chemical tests are out of the question, and biologic 
tests such as the frog eye or muscle strips, are unreliable, since 
substances in the blood other than epinephrin may produce the 
reaction. 2 (5) The injection of epinephrin into the blood causes an 
increased glycemia which, if sufficient in amount, appears as 
glycosuria, and yet investigations upon patients with high arterial 
tension from the standpoint of hyperglycemia have shown indefinite 
results. 

From what has preceded it is sadly evident that we are still 
unable to satisfactorily explain either the cause or the mechanism 
of nephritic hypertension. The whole subject is so complex and 
the evidence at hand so contradictory that judgment is difficult. 
Janeway, than whom no one is better qualified to speak, draws 
the following conclusions: 

1 . Hypertension may arise through purely quantitative reduction 
of kidney substance below the factor of safety. It is difficult to 
conceive of this as other than a vascular hypertonus due to retained 
poisons of some kind. Its clinical paradigm is the hypertension 
accompanying bilateral ureteral obstruction or the unfortunate 
surgical removal of the only functionating kidney. Possibly it is 
one factor which helps to produce hypertension in the contracted 
kidney. 

2. Hypertension may arise in connection with the unknown 
intoxication which causes disturbances of the central nervous 
system, and which we call uremia. This intoxication is not one of 



1 Trendelenburg, W., Ueber d. Beziehungen d. Nebennieren z. normalen Blut- 
druckhohe, Ztschr. f. Biol., 1914, xliii, 155; Hoskins and McClure, The Adrenals 
and Blood-pressure, Arch. Int. Med., October, 1912, p. 343. 

2 Stewart, G. N., So-called Biologic Tests for Adrenalin in the Blood, with Some 
Observations on Arterial Hypertonus, Jour. Exp. Med., 1911, xiv, 377; O'Conner, 
Ueber d. Adrenalingehalt des Blutes, Arch. f. exp. Path. u. Pharmakol., 1912, lxvii, 
195. For other references see .Taneway's article, loc. cit. 



NEPHRITIC HYPERTENSION 281 

retention, in a strict sense, although it is most commonly present 
in those cases of advanced nephritis which manifest marked nitrogen 
retention. Clinically it is associated with severe acute nephritis, 
sometimes at its very onset, besides the subacute and chronic 
inflammatory affections of the kidney. 

3. Hypertension may arise in primary irritability of the vaso- 
constricting mechanism from unknown, probably extrarenal, 
causes which lead eventually to arteriolarsclerosis. In this type the 
disease in the kidney is the sequence, not the cause, of the general- 
ized vascular lesion. When it progresses to a condition of extreme 
atrophy, resulting in the true primary contracted kidney, a renal 
element may be added to the existing hypertension. In some cases 
arteriosclerosis of the larger vessels may spread peripherally and 
produce a similar form of disease. In these forms of primary 
vascular disease it is probable that eventually wide-spread narrow- 
ing of the arterial stream bed in some cases produces a permanent 
organic increase in peripheral resistance. 

Very recently Voegtlin and Macht 1 have succeeded in isolating 
from the blood and serum a crystalline pressor substance, whose 
pharmacologic action is different from epinephrin and from any 
other body hitherto obtained from the blood. It produces marked 
cardiac stimulation and a prolonged vasoconstrictor effect. They 
found that its physical and chemical properties seem "to point to 
its relation to cholesterin on the one hand and to the cortex of the 
adrenal gland on the other." Gubar 2 has shown that the blood-serum 
of nephritics has a pressor effect and Cantieri 3 found that there 
was no relation between high blood-pressure and the cholesterin 
content of the blood. It is quite possible that this new substance 
may prove to be of considerable clinical importance. Occasionally 
hypertension is caused by focal infection, such as pyorrhea, sinusitis, 
chronic tonsillitis, suppuration in the antrum, etc., presumably as 
a result of toxin absorption and renal irritation. The relation of 
hypertensive cardiovascular disease to syphilis has been considered 
under the heading of the latter, p. 213. 

Renal Circulation and Functionation. — Renal functionation is 
extremely sensitive to vascular changes in the kidney. The kidney 
differs from other organs of the body by functionating more or 

1 The Isolation of a New Vasoconstrictor Substance from the Blood and the 
Adrenal Cortex, Presence of the Substance in the Blood and its Action on the Car- 
diovascular Apparatus, Jour. Amer. Med. Assoc, 1913, lxi, 213G. 

2 Russk. Vratch, 1913, xx, 725. 

3 Wien. klin. Woch., October 16, 1913. 



282 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

less constantly and by being frequently forced to do extra work 
by its possessor. According to Tigerstedt, from ten to nineteen 
times more blood passes through the kidneys, despite their small size, 
than through all the other organs combined. 1 The kidney normally 
contains about 1.63 per cent, of the total blood (Ranke). During 
well-marked diuresis it may contain 5.6 per cent. 2 The anatomic 
arrangement of the vessels insures the longest possible blood-path, 
together with a double system of capillaries. The kidney may 
show an increased rate of blood-flow without an increase either 
in volume or in pressure, a fact which Hasebroek uses to substantiate 
his belief in an active vascular diastole. Renal activity is inde- 
pendent of general systemic pressure. 3 Vasoconstriction alone 
may cause a great reduction of blood-flow in the kidney (B. Opitz). 

The secretion of urine varies directly with the pulse pressure. 4 
In fact, a marked increase of pressure may produce albuminous 
urine, and a decrease below a certain point causes anuria. 

It has generally been believed that the circulation through the 
kidneys, as regards vascular dilatation or contraction, depended 
upon the amount of urogenous material in the blood, and that the 
secretion of urine increased with an increased blood-pressure and 
blood-flow. The increased pressure is believed to especially cause 
an excretion of water, the concentration of the urine depending 
upon the activity of the renal epithelium. Hypertension only causes 
a polyuria if the blood contains a definite amount of urogenous 
material. In case of atrophied kidneys with a restricted capillary 
area it is assumed that an increased pressure is required to keep 
up elimination. This view has had very wide acceptance from 
clinicians who believed that a fall of pressure meant diminished 
urine and often led to uremia, and who therefore regarded the 
hypertension as compensatory and necessary. Experimental 
evidence, on the other hand, in a negative way indicates that (a) 
increased renal resistance is not the cause of hypertension ; (b) that 
the latter does not cause an increased blood-flow through the 
kidneys; (c) that hypertension is not accountable for the polyuria. 

The results of experimentation, however, cannot in the present 
state of our knowledge be accepted as equivalent to what occurs 



1 Lehrbuch d. Physiologie des Kreislaufes, Leipzig, 1S93, p. 552. 
- Landergren and Tigerstedt, Skand. Arch. f. Physiol., 1892, iv, 242. 
:i Weber, Arch. f. exp. Path. u. Phar., 1905, vol. liv. 

4 Erlanger and Hooker, Johns Hopkins Hosp. Rep., 1904, xii, 145; Hooker, 
Amer. Jour. Phys., 1910, xxxvii, 24. 



NEPHRITIC HYPERTENSION 283 

in human disease, because the entire problem is extremely complex, 
and because the syndrome which constitutes chronic interstitial 
nephritis has not yet been produced experimentally. ■ 

Clinical Phenomena. — The rise of pressure which occurs in chronic 
interstitial nephritis is generally regarded as a compensatory 
effect. A certain amount of kidney substance has been destroyed, 
but renal elimination must be maintained at any cost, and the 
cost is always a high one. More blood must pass through the 
renal vessels in a given time, and this Nature accomplishes by raising 
the blood-pressure in the renal arteries, which entails an elevation 
of the general systemic pressure. The latter greatly increases 
vascular wear and tear and, when the heart is capable of it, brings 
about a cardiac — chiefly left ventricular — hypertrophy. 

Lawrence, 1 who has recently reviewed this question, finds, 
however, that clinical reports are by no means unanimous in declar- 
ing hypertension to be compensatory and protective, and quotes 
numerous investigators to the effect that a lowering of pressure 
is coincident with symptomatic improvement. Lawrence's own 
studies show that there is no definite relation between changes in 
either the systolic or the diastolic pressure per se and alterations 
in urinary secretion, but that when an increased pulse pressure 
results from a diastolic fall the urinary secretion is augmented. 
This occurred in only half of the cases in which the increased 
pulse pressure was due to a systolic rise. Thus "an increase in 
the caliber of the vascular system seems to be more efficient in 
promoting diuresis than does increased pressure in the aorta and 
its great branches." 

It is the maximum pressure which is chiefly affected in nephritic 
hypertension; the minimum pressure lags behind, thus affording 
a larger amplitude. 2 In nephritic hypertension both the minute 
volume and the systolic output remain practically unchanged (Berg- 
mann and Plesch) ; indeed, they may even be subnormal in spite 
of the increased systolic and diastolic pressures. Nor is the rate 
of flow increased. Even pressures of 200 mm. may be accompanied 
by only a normal rate of flow, while a fall of pressure may actually 
mean an increased rate (Stewart). As a rule the blood-pressure 
increases gradually over a period of years, the individual appearing 



1 The Relation of Hypertension to Urinary Excretion, Amer. Jour. Med. Sci., 
September, 1912, p. 330. 

2 Musser, J. H., Jr., The Relation of High Systolic to Diastolic Pressure, Arch. 
Diagnosis, July, 1914. 



284 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

in perfect health, and is discovered perhaps accidentally while the 
patient consults the physician for some other ailment, or it may be 
that a palpitation of the heart, fulness of the head, gastro-intestinal 
disturbances, or dyspnea on exertion cause him to seek medical 
advice. But high blood-pressure sometimes appears very early 
in cases of acute nephritis. Buttermann in one case observed 
a rise of 50 mm. within forty-eight hours of the onset of albu- 
minuria. 

Lee 1 found renal lesions in 71 per cent, of his autopsied cases 
of hypertension, and of these in 72 per cent, the lesion was atrophic. 
Arteriosclerosis was present in 69 per cent., but in only 1 case 
could all other hypertensive factors be eliminated. Among the 
15 cases in which no renal disease was found, 7 presented cerebral 
lesions. No patient without either nephritis or arteriosclerosis showed 
a blood-pressure of over 200 mm., and all who had a pressure constantly 
or repeatedly above this figure had some renal lesion. 

During four years at the Heidelberg Clinic there were 450 cases 
with a pressure above 140 mm. Among 148 cases a pressure 
over 200 occurred (1 case 272 mm.); of these there were 24 with 
unquestioned and 10G with doubtful nephritic symptoms. There 
were 16 cases which showed no albumin among the above-mentioned 
148. If we consider only the cases having a pressure over 200, 87 
per cent, showed renal changes. Strikingly frequent were the 
arterial changes, both clinically and anatomically. Among 450 
cases of hypertension 44 died; 43 were autopsied with the following 
results; contracted kidney, 10; contracted kidney with general 
arterial sclerosis, 14; sclerosis of the renal arteries, 3; secondary 
contracted kidney, 1; secondary contracted kidney with arterial 
sclerosis, 3; parenchymatous nephritis, 5; arterial sclerosis, 3; 
arterial sclerosis with myocarditis, 2; pyelonephritis, 1; hydro- 
nephritis, 1. In other words, arterial processes played a part in 58 
per cent, of the cases. 2 

Among 550 patients with continuously high blood-pressure, 62 
per cent, of those with readings above 140 showed signs of pro- 
nounced kidney disease, as did also 80 per cent, of those with 
pressures above 160 mm. Of 42 examined postmortem, every one 
showed anatomic changes indicating progressive kidney disease, 
even those in which there had been no clinical evidence of it and 

1 Pathologic Findings in Hypertension, Jour. Anier. Med. Assn., 1911, lvii, 1179. 

2 Schonthaler, Bericht ueber in den letzten 4 Jahren an der Heidelberger Medi- 
zinischen Klinik beobachteten Hypertonien, Dissertation, Heidelberg, 1912, p. 39. 



XE I'll 111 TIC 11 YPEHTENS10N 



285 



in which congested kidney or idiopathic dilatation of the heart 
had been diagnosticated. 1 

Elevation of blood-pressure occurs chiefly in the atrophic kidney 
when the damage is mainly glomerular. It occurs experimentally 
in uranium nephritis, and in such cases cardiac hypertrophy 
has been reported. 2 It may occur in exceptional cases of 
parenchymatous nephritis, hydronephrosis, etc., in explanation of 
which fact we have only to remember that the pathologic renal 
changes are often complex, and the lesions rarely limited exclusively 
to either the epithelial or endothelial structures. 

The feeding of protein bears a direct relation to the amount 
of nitrogen retention in the blood of nephritics, especially in 
interstitial nephritis associated with hypertension. This does not 
occur in passive congestion. Nitrogen retention is often asso- 
ciated with a low phthalein output and increased blood-pressure. 3 

The relationship between the nitrogen content of the blood and 
the degree of blood-pressure is, however, not constant, although 
patients with a high index are more subject to edema, nausea, 
vomiting and uremia. 4 

Hyperglycemia of a slight degree was found by Hopkins 5 to occur 
in many high pressure nephritics, often in association with a low 
phthalein output. There is, however, no definite relation between 
the degree of hyperglycemia and that of hypertension. Most of 
the cases of nephritis without high blood-pressure have a normal 
amount of sugar in the blood. Venous blood-pressure is not increased 
in nephritis until cardiac insufficiency begins. 

Sodium Chloride Metabolism and Blood-pressure. — The elimination 
of sodium chloride from the diet of nephritics is sometimes attended 
by a marked increase of the urinary output. This substance is 
often eliminated with difficulty and its retention in the tissues 
favors the retention of fluid. The effect of sodium chloride on 
blood-pressure is also a variable one. In some cases the institution 
of a salt-free diet will definitely lower blood-pressure while chlorin- 



1 Fischer, J., Relations between Permanently High Blood-pressure and Kidney 
Disease, Deutsch. Arch. f. klin. Med., 1913, cix, Nos. 5-6. 

2 Siegel, W., Ueber experimentale nephritis, Kongr. f. inn. Med., 1907, xxiv, 217. 

3 Hopkins, A. H., and Jonas L., Studies in Renal Function with Special Reference 
to Non-protein Nitrogen and Sugar Concentration in the Blood, Phenolsulphone- 
phthalein Elimination and Blood-pressure, Arch. Int. Med., 1915, xv, 964. 

4 Seymour, M., The Effect of Nitrogenous Waste Products in the Blood in Chronic 
Interstitial Nephritis, Boston Med. and Surg. Jour., 1913, clxix, 795. 

; The Concentration of Blood Sugar in Health and Disease as Determined by 
Bang's Micromethod, Am. Jour. Med. Sci., 1915, cxlix, 254. 



286 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

ization will produce an increase in pressure perhaps associated 
with general fluid retention and edema of the lungs. 1 Indeed it 
has been claimed that hypotensive properties of different medicinal 
substances owe their effects directly to their influence on the 
urinary chloride elimination. 2 This view has been strenuously 
opposed by most investigators. Brodzki 3 was unable to produce 
a rise of pressure in nephritic cases by the administration of sodium 
chloride or meat extracts. (See page 241.) 

Blood-pressure and Urinary Secretion. — The relation between 
blood-pressure and urinary secretion is complex and not altogether 
understood. It has been established, however, that a certain 
minimum pressure is essential to secretion and also an intermittent 
pressure, but above the said minimum pressure the rate of flow is 
milch more important than the actual height of pressure. The 
effect of combined high pressure upon the glomerular structure 
has been described by J. McCrae as follows: 

The capillary coil which we call the glomerulus has a large 
afferent vessel in which blood-pressure is high, and a small efferent 
vessel in which it is low. The glomerulus is therefore much more 
subject to wear and tear due to increased arterial pressure than 
are the tubular capillaries. "The kidney thus resembles a com- 
pound engine, in that most, if not all, the blood goes to the 
high-pressure cylinder, thence much of it goes to the low-pressure 
tubular capillaries, just as the stream, deprived of much of its 
expansive force, goes to the low-pressure cylinder; in all this the 
mechanical advantage is evident." (J. McCrae.) When, however, 
the glomeruli have as a result of incessant wear and tear, undergone 
hyaline degeneration, the high pressure is transferred to the tubules 
which stand this abnormal strain badly, and may rapidly become 
functionally insufficient. Experimentally it has been shown that the 
amount of urine excreted varies directly with the magnitude of 
the -pulse -pressure. Exceptionally sudden vascular pressure changes 
have an augmenting influence. The chloride, urea and total 
nitrogen elimination generally vary with the pulse pressure. Reason- 
ing from the foregoing facts, a drug which will increase pulse 
pressure without markedly lowering the general blood-pressure or 

1 Lowenstein, Ueber Beziehung zw. Kochsalzenthalt u. Blutdruck bei Nieren- 
kranken, Arch. f. exp. Path., 1907, lvii, 137. 

2 Renean, A., Rapports de la Chlorure uninaire avec 1' hypertension arterielle, 
etc., These de Lyon, 1909. 

3 Exper. Untersuch. u. d. Verhalten d. Blutdrueks u. d. Einfluss der Nahrung 
auf denselben f. chronischer Nephritis, Deut. Arch. f. klin. Med., May, 190S. 



NEPll III TIC II YPERTENS1 ON 287 

unduly constricting the renal arterioles, should be a good diuretic. 
1 HgitaJis and strophanthus fulfil these requirements and their 
diuretic effect appears to be due directly to their effect on pulse 
pressure (Gesell). 1 

In disease the relation between urinary output and blood-pressure 
is not constant. This may be due to nervous influence by virtue 
of which the supply of renal" blood does not stand in proportion 
to the general blood-pressure. It cannot be due to exacerbations 
of local inflammation because, as Herringham 2 declares, the "ap- 
parent discrepancy alters from day to day in so inconstant a manner 
that no fresh access of inflammation can explain it, and in the 
second place we should expect, if that explanation were true, that the 
albumin should vary with the inflammation. A fresh attack would 
probably result in an increase of the albumin. But no such variation 
takes place constantly in the albumin. The decrease of urine is not 
always accompanied by an increase in the proportion of albumin." 

As a general rule, however, low-pressure cases excrete less urine 
than high-pressure cases, and the most satisfactory diuretics do 
not have a depressor action. The complexity of the problem and 
the likelihood that numerous factors have a variable effects on 
blood-pressure is shown by the following observations: 

"In a case of -nephritis with albuminuria and persistently high 
arterial pressure studied by Stewart 3 the pressure was reduced by 
forced breathing. This effect was in part due to an increased 
elimination of carbon dioxid by the lungs and to mechanical inter- 
ference with the circulation. The administration of large doses of 
sodium bicarbonate was also associated with a marked fall of 
pressure. In another case the withdrawal of cerebrospinal fluid 
reduced the arterial pressure apparently by lowering intracranial 
pressure. No pressor substance could be demonstrated in the 
cerebrospinal fluid." 

The Complications of Hypertension. — I. Uremia. — Chronic uremia 
is associated with high, acute uremia with very high, blood-pressure. 
The latter is sufficiently marked to be of great diagnostic value. 
The increment in pressure depends largely on the height of the 
preceding average pressure. When this has been low, increases of 
100 per cent, are not unusual. 

1 The Relation of Pulse Pressure to Renal Secretion, Amer. Jour. Physiol., 1913, 
xxxii, 71. 

2 Kidney Diseases, London, 1912, p. 220. 

J So-called Biological Tests for Adrenalin in Blood, with some Observations on 
Arterial Hypertonus, Jour. Exp. Med., 1911, xiv, 4. 



288 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

The cause of these sudden increments of tension is not and 
cannot be known until the causes of hypertension in nephritis and 
the nature of uremia have been elucidated, but the hypothesis that 
many of the uremic symptoms are the direct result of abnormal 
local pressure relations is extremely plausible.- 

The symptoms of uremia are well known and require no special 
consideration. All of the transient nervous phenomena described 
under Cerebral Vascular Crises (see page 260) may result from 
uremia. Vascular spasm may be the etiologic factor in either case. 

II. Paroxysmal Dyspnea. — Paroxysmal attacks of increased 
tension and dyspnea are not uncommon in arteriosclerotic subjects, 
especially with renal involvement. It is quite likely that these 
phenomena are due to irritation or disease of the depressor nerve 
in the aorta, hence they are encountered especially in cases of 
syphilitic aortitis. Bittorf 1 has reported degeneration of the depressor 
nerve in two patients with aortic sclerosis (aged forty-three and 
fifty-six years) associated with hypertension and cardiac hyper- 
trophy. 

"Having still more important bearing on this subject are some 
old experiments of Francois Frank 2 on aortic reflexes. By irritating 
the inner surface of the aorta of dogs he was able to produce quite 
constantly certain respiratory phenomena. These consisted of 
three types: (1) Sudden apnea with the respiratory muscles in 
spasm either during the inspiratory or expiratory phase, or apnea 
with general inhibition of all respiratory movements; (2) tachypnea, 
without severe constitutional symptoms, and (3) a slow dyspnea 
of severe and grave form. The cause of this dyspnea he showed 
quite plainly was spasm of the bronchial musculature. He believed, 
too, that there was coincident contraction of the pulmonary artery. 
Associated with this type of dyspnea was a contraction of the 
peripheral vessels and rise of blood-pressure. Occasionally a spasm 
of the laryngeal muscles occurred. In other cases he was able to 
produce all the signs of aortic insufficiency (the capillary and 
collapsing pulse) save a diastolic murmur through irritation of 
the root of the aorta and without injury to the sigmoid valves. 
Stewart 3 has observed this last phenomenon and considers it as a 
reflex from the root of the aorta, and in some experiments in which 
aortic insufficiency was performed on dogs I have repeatedly 

1 Deut. med. Woch., 1910, No. 46. 

2 Arch, de Physiol., 1890, series 5, ii, 508 and 547; Jour, de l'anat., 1S77, xiii. 545. 

3 Archiv. Int. Med., 1908, i, 102. 



NEPHRITIC HYPERTENSION 289 

confirmed this observation. That Frank's respiratory phenomena 
have not been noted since is almost certainly due to the method of 
experimentation, for in Stewart's experiment, and in those which 
others have performed, full ether anesthesia or artificial respiration 
was employed. 

"It is thus evident that disturbing reflexes may be set up experi- 
mentally in animals by irritation of the root of the aorta, and there 
is no reason to suppose that the same thing should not be true for 
man. The dyspnea caused by bronchiospasm, and the contraction 
of the peripheral arteries producing heightened blood-pressure in 
the experimental animal is a close reproduction of the paroxysmal 
dyspnea as it occurs in syphilitic aortitis, and it seems quite justi- 
fiable to suggest that the two conditions are the same. It would 
be difficult to explain the increase in blood-pressure which occurs 
during these attacks in man on the presence of pain or of cyanosis, 
for pain is frequently absent and dyspnea may continue for some 
time (fifteen to thirty minutes) after the sudden drop in blood- 
pressure which comes with the relief of acute symptoms. Our 
observations, therefore, seem to lend strong support to the idea 
that these symptoms are dependent on a reflex generated at the 
root of the aorta by the syphilitic inflammatory process. 1 The 
attacks have been found to consist of three phases: (1) A very 
high systolic and diastolic pressure 210-190; (2) falling pressures 
in which the diastolic may remain disproportionately high (a bad 
sign) ; (3) a gradual return to the normal. 2 

Paroxysmal dyspnea may also occur when the cerebrospinal 
pressure becomes too high. Such attacks may be associated with cere- 
bral symptoms — headache, vomiting, vertigo, and with subjective 
oppression and respiratory acceleration, but without preexisting 
asthmatic symptoms. It has been suggested that although certain 
forms of non-cyanotic dyspnea frequently described as "renal" 
or "cardiac" are associated with high blood-pressure, they are 
basically due to renal defects and are directly dependent upon an 
acid intoxication. 3 Peabody's 4 studies showed that when acidosis, 
as indicated by the alveolar carbon dioxid tension, occurs in cardiac 
and cardiorenal disease, it is associated with an increased stimula- 

1 Longcope, Arch. Int. Med., January, 1913. 

2 Amblard, L. A., La Tension Arterielle dans l'oedem aigu du Poumon, Presse 
Medicale, 1911, xix, 657. 

3 Lewis, Ryffel, Wolf, Cotton, and Barcroft, Observations Relating to Dyspnea 
in Cardiac and Renal Patients, 1913, Heart, v, 45. 

4 The Effect of Carbon Dioxid in the Inspired Air on Patients with Cardiac Disease, 
Arch. Int.. Med., 1915, xvi, 846. 

19 



290 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

bility to carbon dioxid in the inspired air. In patients of this class 
dyspnea occurs more readily than in normal subjects or in patients 
without acidosis. He was led to conclude that while acidosis is 
probably not the only factor in cardiorenal dyspnea it may play a 
considerable role. A lowering of the blood-pressure often brings 
relief. 

When dyspnea (asphyxia) is the cause of the hypertension, 
bleeding, digitalis and general measures are indicated. In the 
Cheyne-Stokes type of breathing, lumbar puncture, which relieves 
cerebrospinal pressure, is in order, although it has not much effect 
upon the general pressure. Morphin is useful in either type. 1 

III. Cheyne-Stokes Respiration. — Cheyne-Stokes breathing is 
frequently encountered in association with arterial hypertension. 
This symptom when occurring in association with experimentally 
increased intracranial tension has been shown by Cushing 2 to be 
accompanied by high pressure during hyperpnea and low pressure 
during apnea. The importance of this fact from a clinical stand- 
point in order to differentiate between Cheyne-Stokes respiration 
with and without increased intracranial pressure was demonstrated 
by Eyster; 3 the findings of the latter were corroborated by Pollock, 4 
who explains the exact mechanism of the symptoms as follows: 

"The intracranial tension being higher than the general blood- 
pressure, cerebral anemia exists and apnea is present. The vaso- 
motor centres are automatically stimulated to raise the general 
blood-pressure in an effort to produce an equilibrium between it 
and the intracranial tension. As the general blood-pressure rises, 
respiratory movements recommence; at their height the vasomotor 
centres are no longer stimulated, the general blood-pressure again 
falls, and the respiratory movements diminish and finally cease." 

Hyperpnea is associated with increased amplitude of the apex 
beat, and the pulse rate increases with the rise of blood-pressure. 
Arhythmia and prolongation of the a-c interval may also occur. 
Symptomatic relief often follows lumbar puncture, which tem- 
porarily reduces intracranial tension. 

From Eyster 's investigations it would seem that the stimula- 
bility of the respiratory centre is at a permanently low level, which 
requires an abnormally intense stimulus to produce a response, 
the stimulus being supplied by the toxic products which have accu- 

1 Pal, J., Paroxysmale Hochspannungsdyspnea, Vienna, 1907. 

2 Amer. Jour. Med. Sci., 1902, cxxiv, 375; 1903, cxxv, 1017. 

3 Johns Hopkins Hosp. Bull., 1906, xvii, 296. 

* Blood-pressure in Cheyne-Stokes Respiration, Arch. Int. Med., 1912, ix, 406. 



NEPHRITIC HYPERTENSION 291 

mulated in the blood through apnea and low pressure. The admin- 
istration of C0 2 toward the end of the hyperpneic period has in 
one instance prevented the recurrence of the apneic periods. 1 

IV. Acute Pulmonary Edema. — Pulmonary edema may occur 
in patients with chronic vascular hypertension. Attacks are 
'preceded by a rise of both systolic and diastolic pressures. During 
the attack the maximum pressure, which has been very high (240 
to 280 mm.), falls greatly, the minimum slightly. At such times 
venesection, although often beneficial, exerts but little effect on the 
pressure. After the attack, in cases which recover, pressure rises 
gradually to the normal. These symptoms, as was first shown 
by Welch and Cohnheim, 2 find their explanation in the fact that 
a temporary left ventricular failure, while causing a fall in the 
systemic circulation, produces a great stasis rise in the pulmonary 
vessels which the right ventricle is no longer able to overcome, and 
which either in isolation or in association with toxins leads to serious 
oozing or vascular rupture into the pulmonary parenchyma. 
Experimentally, epinephrin may produce pulmonary edema through 
vascular degeneration, alveolar inflammation, and increase of 
pressure. It may also be produced by clamping the aorta or com- 
pressing the left ventricle. The primary disturbance, therefore, 
seems to be some influence on the nervous system which interferes 
with the normal regulation of the correlated vascular tension, 
heart action, and respiration in the case of an already diseased 
heart. 3 It has been suggested that attacks of pulmonary edema in 
nephritics are the result of an effort on the part of the system to 
rid itself of urea and chlorides. 4 Among 405 cases of pulmonary 
edema postmortem, Coplin found renal lesions in 333. An early 
and marked fall of pressure may result from cardiac exhaustion. 

Prognosis. — Chronic arterial hypertension is a serious condition 
which generally spells chronic interstitial nephritis. The degree 
of hypertension bears no constant relation to the severity of the 
nephritis as determined by the routine urine examination, the 
phthalein elimination or the amount of nitrogen retention. The 
mildest cases may show the highest pressures. 

1 Observations on Two Cases of Cheyne-Stokes Respiration, Jour. Physiol., 
1906, xxxiv, 6. 

2 Gesammte Abhandl., Berlin, 1885, p. 594. 

3 Amblard, A., Presse Medicale, August 12, 1912; Petren, Berlin, klin. Woch., 
December 27, xlvi. 

4 Lesieur, Froment, and Rochaix, Oedemes aigus du poumon. Comparison du 
taux de l'uree et de chlorures dans le serum sanguin et dans l'expectoration, Soc. 
med. des Hop., Paris, November 19, 1909. 



292 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

The absence of hypertension in a case which presents the other 
clinical evidences of chronic interstitial nephritis suggests the 
existence of a tuberculous, syphilitic or amyloid lesion of the kidney. 
When associated with severe cardiac symptoms and retinal hemor- 
rhages a lethal termination may be expected within a few years. 
The teaching was formerly current that nephritic retinal hemor- 
rhages were invariably followed by death within a period ranging 
from six months to two years. While this is doubtless true where 
hemorrhages are severe and recurrent, yet in the case of well-to-do 
patients who can and will modify their manner of life, there can be 
no question that such a prognosis is unnecessarily austere. Many 
cases of retinal hemorrhages are not seen by the ophthalmologist 
in their early stages. Plenty of cases are on record in which patients 
have lived ten years or more after the onset of nephritic retinal 
hemorrhages. It is a common observation that patients having a 
pressure ranging around 180 mm. (systolic) and 110 mm. (diastolic) 
without marked urinary findings, or of ocular or cardiac symptoms, 
may live for many years. Strauss 1 has reported the case of a patient 
who lived five years with a systolic pressure ranging between 260 and 
270 mm. Hg. (See page 131.) Hypertensive cases are apt to have 
exacerbations of pressure (200 mm. and over) associated with more 
or less troublesome symptoms — insomnia, nervousness, irritability, 
weakness, fatigue, inability to concentrate attention, mental depres- 
sion, dyspnea, precordial oppression, etc. — which will under appro- 
priate treatment subside. Such cases are regarded as bad insurance 
risks, and justly so, and yet with an intelligent comprehension of 
their condition and a willingness to curtail the expenditure of 
energy, they may lead lives of usefulness and comparative comfort 
for many years. These statements are borne out by Paessler's 2 
graduated nephrectomy experiments, in which he showed that 
years of comfort and activity were compatible with a pressure of 
200 to 250 mm. The prognosis, therefore, often hinges quite as 
much on the individual as on the disease. The occurrence of well- 
marked edema in hypertensive cases is more serious than in cases 
of valvular disease. The following rides, as laid down by Lichty, 3 
indicate the general lines upon which a prognosis may be based: 

"1. Where hypertension exists with but little or no recognizable 
disturbed function of other organs the outlook is most favorable. 

1 Deut. med. Woch., 1915, xli, No. 1G. 

2 Samml. klin. Vortrage, No. 408. 

3 Hypertension: A Report of Cases under Prolonged Observation, and a Protest 
Against Some Ideas, Am. Jour. Med. Sci., May, 1913. 



NEPHRITIC HYPERTENSION 293 

(2) Where it is associated with marked disturbance of any one 
other organ alone it is more serious. (3) Where it is associated 
with great defect of several other organs, such as kidney insufficiency, 
cardiac insufficiency, cirrhosis of the liver, and lesions of the gastro- 
intestinal tract, the prognosis is most serious. (4) When the hyper- 
tension is associated with symptoms and physical signs which 
disappear after a more or less active and prolonged treatment which, 
however, fails to lower the tension, a favorable prognosis is not 
unwarranted. Such cases are rather frequent, and I believe it is 
just as unreasonable to take an unfavorable view of them as it is 
to predict a speedy fatality in all cases of pulmonary tuberculosis 
where the bacilli are found in the sputum. (5) When the tension 
is found in connection with changes in organs producing such 
extreme symptoms as dropsy, ascites, cyanosis, and orthopnea, 
and when these symptoms cannot be relieved, whether the tension 
is modified or not modified by heroic treatment covering five to 
eight weeks, then defeat is sure." 

As to the cause of death in hypertension, this may result from 
apoplexy, uremia, angina pectoris, broken cardiac and vascular 
compensation, or from intercurrent disease. Among 565 cases of 
renal disease at St. Bartholomew's Hospital 209 died from renal 
disease, as follows: 

Sudden death without any other sufficient cause 9 

From uremia 28 

From cerebral hemorrhage 82 

From cardiac failure 90 

209 

The following tables are taken from Janeway's article based on 
a study of 100 cases with a blood-pressure of or above 170 mm. Hg. 

The Age of the Patients. 

Below 20 years 2 cases, about 2 per cent. 

20 to 29 years cases, about per cent. 

30 to 39 years 3 cases, about 3 per cent. 

40 to 49 years 24 cases, about 21 per cent. 

.50 to 59 years 39 cases, about 34 per cent. 

60 to 69 years 32 cases, about 28 per cent. 

70 and over 14 cases, about 12 per cent. 

114 



294 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 



The Duration of the Illness in Relation to the Causes of Death. 

Duration. 
Average. Longest. Shortest. 

Cases. Years. Months. Years. Years. Months. 



Causes of death 
Cardiac insufficiency 
Acute uremia 
Chronic uremia 
Cerebral apoplexy . 
Angina pectoris 
Acute edema of lungs 



26 3 10 10 .. 4 

14 3 .. 8 .. 5 

21 3 1 7 4 

14 4 6 11 .. 11 

3 4 3 6 3 6 

4 3 .. 4 1 8 



The Immediate Cause of Death. 

Gradual cardiac insufficiency 29 

Uremic convulsions or sudden coma 15 

Chronic uremia 20 

Uremic psychosis " 1 

Cerebral apoplexy 14 

Acute edema of the lungs 4 

Angina pectoris 3 

Sudden death (unclassified) 4 

Progressive anemia 2 

Acute pneumonia • 4 

Unrelated diseases 4 

100 

Stone 1 has called attention to the fact that the cardiovascular 
type of hypertension can be differentiated from the nephritic, or as 
he prefers to designate it, the cerebral type, by the pulse pressvre 
and the cardiac load (see page 267). Thus in arterial hypertension 
associated with valvular or myocardial lesions, the diastolic pressure 
is persistently lower than in the cerebral type. Hence with an 
equal systolic pressure the overload is increased — in 24 patients 
to an average of 46 per cent. Such a differentiation has a good 
deal more than an academic importance because both prognosis, 
therapy and mode of death vary very distinctly in the two types. 

Hypertensive disease as seen in hospitals presents a very different 
picture from that seen in private practice. In the former instance 
we see chiefly the terminal stages. Since the alleviation of symp- 
toms as well as the prolongation of life depends mainly upon an 
early recognition of the condition, it is important to know the early 
symptoms from which patients have suffered. These are shown 
in the following table from Janeway's recent article. 2 

1 The Differentiation of Cerebral and Cardiac Types of Hyperarterial Tension 
in Vascular Disease, Arch. Int. Med., 1915, xvi, 775. 

2 A Clinical Study of Hypertensive Cardiovascular Disease, Arch. Int. Med.. 
1913, xii, 755. 



NEPHRITIC HYPERTENSION 



295 



The Relation of Prominent Early Symptoms with High Blood-pressure 
to Causes of Death. 



Symptoms. 


Causes of death. 




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Gradual cardiac insuffi- 


9,9 


7 


2 





1 





7 


2 


1 


2 


3 


3 


Uremic convulsions or 
sudden coma .... 


15 


5 


1 


2 


3 





11 


8 


5 


4 


5 


1 


Gradual uremia 


20 


6 


2 


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2 


2 


2 


2 


1 


4 





4 


Cerebral apoplexy or its 
results 


14 


1 


1 





2 























Angina pectoris 


3 


2 


2 


1 


1 


1 


1 











1 


1 


Edema of the lungs 


4 


3 


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1 


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Other causes .... 


15 


48 


24 


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15 


11 


32 


15 


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13 


14 


16 




100 



It is evident from the foregoing tables that cardiovascular failure 
is the commonest cause of death, while uremia and apoplexy are 
frequent, and angina pectoris is relatively rare. Early ocular 
changes are often followed by uremic death. A certain number 
of cases die as the result of a progressive anemia which has its 
basis in the renal lesion, and a small number from acute pulmonary 
edema. 

Janeway's recent careful analysis of cases of hypertensive cardio- 
vascular disease showed that the average duration of life in these 
cases after the onset of hypertension was four years for men and 
five for women. During the first five years one-half the cases 
died, one-quarter lived between five and ten years, and the remainder 
over ten years. He further found that definite prognostic con- 
clusions, based upon the actual height of the pressure found, were 
unwarranted. 

Certain conclusions may generally be drawn as to the ultimate 
manner of death from the history and the physical signs. Thus 
the early onset and predominance of dyspnea or other symptoms 
of cardiac weakness indicates " a more than 50 per cent, probability 
of an eventual death by cardiac insufficiency." The occurrence 
of anginoid pain may be similarly interpreted, although only one- 
third of these cases actually die in a paroxysm of angina pectoris. 
In contrast to these cases patients with polyuria, especially if 



296 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

nocturnal, and those with headaches present on waking and 
gradually disappearing, will in about 50 per cent, of instances die 
of uremia. Progressive or marked loss of weight is a bad symptom 
( Janeway) . 

Total number of As a first 

Symptoms. patients. symptom in 

Dyspnea (on exertion and paroxysmal) .... 20 6 

Anginoid pain 16 6 

Edema of lungs 2 

Palpitation 13 8 

Edema of the legs 8 1 

General edema 1 1 

Polyuria 6 2 

Retention of urine 2 2 

Headache 12 1 

Vertigo 9 3 

Hemiplegic attacks .5 1 

Transient coma 1 1 

Uremic convulsion 1 

Drowsiness 1 

Visual disturbances 1 

Pains (mainly neuralgia) 8 3 

Fatigue (physical and mental) 6 1 

Hemorrhages 3 

Loss of flesh 2 

Gangrene of extremities 1 1 

Intermittent claudication 4 1 

Cough 1 

Diabetes 10 6 

Albumin and casts (accidental discovery) ... 3 3 

Cardiac disturbance (accidental discovery) . . 2 2 

High blood-pressure (accidental discovery) . . 1 1 

Acute Nephritis. — Even in children acute nephritis often pro- 
duces a marked elevation of blood-pressure which is of distinct 
diagnostic value, but the rise of pressure does not always occur. 
The pressure may vary according as the glomeruli or tubules are 
chiefly involved. In some cases the amount of blood or albumin in 
the urine seems to bear a relation to the height of the pressure. 
The mean average pressure is not so high as in chronic nephritis, 
and during the height of some infectious fevers the blood-pressure 
rise entailed by the nephritis may be more or less counterbalanced 
by the hypotensive effect of the febrile toxemia. Cardiac hyper- 
trophy may be noticeable in children and young adults four weeks 
after the onset of scarlatinal nephritis. 1 Rolleston found a tem- 
porary rise of pressure in 12 out of 33 such cases. 

Mercurial Poisoning. — Poisoning with the mercurial salts 
produces renal necrosis associated with anuria. Janeway and 

1 Friedliinder, Arch. f. Physiol., 1881, p. 168. 



NEPHRITIC HYPERTENSION 297 

Miiller have reported cases of bichloride poisoning with increased 
blood-pressure (170 mm.) until the terminal fall occurred. 1 

Polycythemia. — Arterial hypertension occurs in some cases of 
polycythemia; indeed, a special type of this disease is often alluded 
to as "polycythemia hypertonica. The fact that increased blood- 
pressure is not a constant finding shows that the origin of this 
symptom cannot lie in increased hemic viscosity, which is present 
in all cases, and which is doubtless often counterbalanced by 
reflex vasodilatation. Ordinary hypertension has no direct or 
constant relation to the erythrocyte count. 2 

In Lucas's 3 collection of 179 cases the blood-pressure was reported 
in 66 instances as follows: 

Cases. 

Blood-pressure, 145 to 170 23 

180 to 200 13 

210, 235, 240, and 310 (one each) 4 

" " 220 3 

200 2 

"The blood-pressure is usually above normal in cases showing no 
splenomegaly (Geisbock's polycythemia hypertonica)." Miinzer 
suggests that polycythemia may result from arteriosclerotic changes 
in the hemopoietic organs, which reflexly bring about an increased 
blood-pressure and increased functional activity. 

Arterial Hypertension and Hemic Viscosity. — Martinet 4 has 
studied the pressure-viscosity relation in a large series of cases, 
and based upon this investigation classifies them as follows: 

1. Eusystolic type, in which the relation between maximum 
pressure and blood viscosity yields a quotient close to 4 (3.8 to 
4.5). These cases even if the pressure is abnormal possess no 
serious renal nor cardiac lesion. 

2. Hypersystolic type, with a sphygmoviscometric index greater 
than 4.5, an increased tension with a lowered viscosity. These 
cases have sclerotic kidneys, left ventricular enlargement, polyuria, 
hydruria, and a tendency to vascular rupture. 

3. Hyposystolic type, index less than 3.5, low tension and high 

1 Janeway, T. C, Nephritic Hypertension, Amer. Jour. Med. Sci., May, 1913, 
651. Miiller, F., quoted by C. Thorel, Path. d. Kreislaufsorgane, Ergebn. d. allg. 
Pathol, u. path. Anat,, 1910, xiv, 133. 

2 Moller, Deut. med. Woch., October 29, 1908, xxxiv. 

3 Erythremia or Polycythemia with Chronic Cyanosis and Splenomegaly, Arch. 
Int. Med., 1912, x, 597. 

4 Pressions arterielles et viscosite sanguine (circulation, nutrition, diurese), Paris 
(Masson), 1912. 



298 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

viscosity. Venous stasis: emphysema, tuberculosis, mitral lesions, 
cyanosis, dyspnea, enlargement of right heart. 

He believes that in the second type the hypertension begins 
as an increased viscosity (from overnutrition), which falls when 
the kidneys begin to fail and the blood becomes more dilute. He 
therefore distinguishes two classes of hypertension: 

(a) Simple hypertension (hyperviscosity). 

(b) Cardiorenal hypertension (hypoviscosity), and considers 
that both prognosis and treatment are quite different in each case. 
Thus in two cases the iodides increased pressure, dropsy, and 
albuminuria, Class (b), while the iodides proved beneficial in Class 
(a). He further suggests that much light may be thrown upon 
the action of certain drugs (purgatives, diuretics) and other thera- 
peutic measures (hydrotherapy, etc.) by a study of the sphygmo- 
viscosity index. 

Pellissier's 1 studies lead him to believe that in cardiac disease 
and in gestational toxemia a fluctuating blood-pressure associated 
with an increased hemic viscosity is of very serious import and in 
pregnancy often an indication for immediate active treatment. 

1 Arch. Mens. d'Obstet. et de Gyn., 1915, iv, No. 5. 



CHAPTER XIII. 
THE TREATMENT OF ARTERIAL HYPERTENSION. 

Hypertension per se is not an indication for treatment except 
along preventive lines any more than is the presence of a heart 
murmur. Hypertension is one of Nature's methods of compensating 
circulatory or visceral deficiency, and in the carrying out of her 
purpose she can fortunately not often be thwarted. Reduce the 
pressure in a case of Bright's disease by violent means, such as 
the nitrites, if you will. After a very brief space of time the pressure 
will rise to its former height. The direct reduction of blood-pressure 
by means of drugs or otherwise is a procedure which should only 
be undertaken after the most careful consideration of the case 
from all its aspects. We must never thoughtlessly or ruthlessly 
interfere with Nature's delicately balanced mechanism of com- 
pensation. Only in the face of impending circulatory failure or 
vascular rupture or temporary pain is direct treatment indicated. 
On the other hand, in arterial hypertension, as Langdon Brown 
has aptly put it, "the patient is living too close to the limits of 
his cardiac reserve," and often a very high pressure can be more 
or less reduced without producing any deleterious results and 
with marked symptomatic amelioration, to say nothing of the 
saving of cardiovascular wear and tear. Just how much pressure 
lowering is possible and desirable must be determined for each 
individual case, and in practically no instance is such an effect 
to be sought merely by the administration of drugs. Treatment 
is generally much more satisfactory and its effects more lasting 
in cases showing only moderately increased pressure. This has 
been well expressed by Brooks, in saying that hypertension is not 
pathologic but is usually, if not always, physiologic in import; 
that it tends to prolong life rather than to shorten it, and that 
when its causes cannot be removed it should not be treated but 
maintained. 

The reduction of vascular hypertension relieves the heart of an 
immense amount of work — entirely unnecessary work in cases in 
which the high arterial pressure results from the toxic factors 
attendant upon a faulty mode of living. 



300 TREATMENT OF ARTERIAL HYPERTENSION 

"The heart, beating at the rate of 70 times a minute, i. e., 4200 
times an hour, 100,800 times daily, and 36,792,000 times annually, 
would pump on an average 2| ounces of blood at each contraction, 
175 ounces a minute, 6564 pounds an hour, or 7| tons a day," 
which "is equivalent to lifting one ton 122 feet high." 1 

Since about 10 pounds of blood are pumped by the heart per 
minute it is self-evident that an increase of pressure ranging between 
10 and 50 mm., not to mention higher figures, must call for the 
expenditure of an enormous amount of cardiac work. Further- 
more, the heart which is called upon to meet such demands is often 
already affected by arteriosclerotic changes. The wear and tear 
on the vascular system is of course a no less important factor. 
Dilatation of the aortic arch, even in nori-syphilitics under fifty 
years of age is of frequent occurrence in cases of nephritic hyper- 
tension. 2 The entire hydrodynamic system is working under a 
continuous condition of forced draught. Brunton has suggested 
that hypertension does harm not only by interfering with tissue 
nutrition but also by hindering the vascular supply of the arteries 
themselves; the vasa vasorum being compressed between the 
intima and the adventitia of the arterial wall, whereas the alter- 
nate contraction and expansion which occurs in health, exercises 
an effect like massage which favors the nutritional flow. 

The Direct Reduction of Blood-pressure. — Blood-pressure should 
very rarely be directly reduced by means of drugs or venesection 
except in case of emergency. The term emergency in this connection 
includes: 

1. Cases with or without excessively high pressure (200 mm. +) 
in which owing to the presence of symptoms such as vertigo, head- 
ache, numbness, tingling, loss of power, mental confusion or actual 
palsy, an apoplexy is feared. Venesection is the method of choice. 

2. Cases with threatened or actual angina pectoris. Here the 
nitrites, especially nitrite of amyl, are useful. 

3. Cases with high pressures in which a cataract extraction is 
to be performed. Sodium nitrite or erythrol tetranitrate will lower 
blood-pressure and diminish the risk of intra-ocular hemorrhage. 

In addition to the foregoing types, Nicholson 3 has suggested the 
use of the nitrites in hypertension cases about to be anesthetized. 

1 Pope, C, Month. Cyclop, and Med. Bull., January, 1910. 

2 Smith, W. H., and Kilgore, A. R., Dilatation of the Arch of the Aorta in Chronic 
Nephritis with Hypertension, Am. Jour. Med. Sci., 1915, cxlix, 503. 

3 The Clinical Significance of Blood-pressure, Med. Record, March 20, 1915. 



DIRECT REDUCTION OF BLOOD-PRESSURE 30] 

This would, however, seem of questionable advisability owing to 
the danger of increasing "shock" (see page 37S). 

There are often two factors concerned in the production of arterial 
hypertension: (1) A basic or essential factor, the point to which 
pressure must be raised to maintain metabolism, and (2) a super- 
added or toxic factor which results from faulty habits of life. It 
is the latter only which we are justified in treating. Ordinarily 
a pressure of 190 mm. or over is an absolute indication for entire 
cessation from work, and generally rest in bed, at least until the 
case has been carefully studied. 

The following history is illustrative of what may be accomplished 
in cases of hypertension: 

Mr. B., aged sixty-one years, high-strung, intellectual, always 
a hard worker, president of a large manufacturing company, 
presented himself in 1908 complaining of fatigue, nocturnal mic- 
turition, headaches and palpitation, loss of weight, and anginoid 
attacks. Blood-pressure: systolic, 200; diastolic, 120 mm. 

The arteries were very sclerotic, hard, and tense, the temporal 
vessels prominent, the eyes injected, the heart enlarged to the 
left with aortic accentuation, a systolic mitral murmur, and a 
reduplicated first sound. Urine: trace of albumin with hyaline 
casts. 

He has intelligently cooperated in carrying out the treatment, 
which consisted in lessening his working hours, avoiding hurry 
and worry as much as possible, relegating all unessential work and 
needless telephone calls to others. Moderation in diet and rest in 
the recumbent posture late each afternoon. Occasional sweat 
baths, with spinal massage. 

In 1915 he is comfortable, puts in a long day's work, but realizes 
his limitations and submits to them. Blood-pressure, 165 to 75 mm. 

He occasionally has hypertensive attacks brought on by undue 
strenuosity which yield to full doses of nitrites, purgation, rest in 
bed, and a milk diet, but, on the whole, feels vastly better and 
accomplishes essentially as much as he did six years ago. 

The treatment of nephritic hypertension is fraught with difficulties 
and requires the best of judgment. High blood-pressure leads 
to cerebral hemorrhage and cardiovascular failure, but high pressure 
is compensating and necessary; if reduced too much the patient 
is apt to suffer from insufficient elimination, which may lead to 
uremia, and from nutritional failure due to loss of capillary pressure. 

Generally speaking, the first step is to secure rest and place the 



302 TREATMENT OF ARTERIAL HYPERTENSION 

patient upon a milk and farinaceous diet. Attention to the intestinal 
tract is extremely important. Regular and free evacuation of 
the bowels is essential. This can generally be accomplished by a 
judicious regulation of diet, fluid intake, and exercise. When drugs 
are required agar-agar, cascara, and other mild laxatives are often 
useful. The occasional employment of blue mass or calomel 
followed by a saline is often attended with excellent results. We 
cannot subscribe with enthusiasm to the laudatory results which 
are said to follow the use of the so-called intestinal antiseptics. 
The use of some of the various forms of fermented milk seems to 
be beneficial, chiefly, however, if other forms of dietary indulgence 
be limited. As has been pointed out there are two main groups 
of hypertensive cases : (1) those presenting chiefly cardiac symptoms 
and usually dying a death from cardiac decompensation, and, 
(2) those with renal symptoms who die with uremic manifestations. 
The treatment of these two types is somewhat different. In the 
former dietary restrictions and eliminative treatment are less 
important, while digitalis and Xauheim baths are more indicated. 
In the latter diet, purgation, sweat baths, etc., are more essential. 

Some but by no means all the headaches of nephritis are due to 
high blood-pressure, and such cases as are, do not yield readily to 
therapy. Certainly direct treatment of the blood-pressure is 
neither justifiable nor successful, unless there is a distinct element 
of toxic vascular spasm which should be relieved by purgation or 
other eliminative means. The urgent symptoms of uremia are 
sometimes satisfactorily relieved by lumbar puncture and the 
withdrawal of cerebrospinal fluid or by venesection. 

Purgation. — Although drastic purgation has long been used for 
conditions associated with marked edema, ascites, and anasarca, 
the advisability of such therapeusis in cases of cardiac weakness 
has been questioned. With a view to investigation of this problem, 
Neilson and Hyland 1 have carried out experiments with the blood- 
pressure, etc., after the use of different cathartics. 

After two doses of a purgative given in the morning, before 
food, the systolic pressure, which was chiefly affected, showed an 
average lowering of 17 per cent, (the diastolic S per cent., the 
pulse pressure 24 per cent.), while the pulse rate increased 14 per 
cent. Symptoms such as vertigo, chilliness, cold extremities, 
dyspnea, clammy skin, etc., were observed. Hypertensive cases 

1 The Effect of Strong Purging on Blood-pressure and the Heart, Jour. Amer. 
Med. Assoc, 1913, lx, 436. 



SLEEP 303 

showed the most marked results, and in these arhythmia occa- 
sionally occurred. 

The results are presumably due to (1) loss of fluid from the 
blood; (2) unequal distribution of fluid, the splanchnic area being 
chiefly affected, and a condition comparable to the experimental 
section of the splanchnic nerves having been induced; (3) cardiac 
weakness due to the small quantity of blood which the heart has 
to handle, increased viscosity; (4) the absorption of mineral salts 
from salines may have a direct action on the heart or its nervous 
mechanism. The fact that the pulse rate is sometimes decreased 
after such purgation despite the lowered blood-pressure tends to 
support this hypothesis. 1 

It was found that compound jalap powder produced a more 
marked, constant, and prolonged fall of pressure than the salines, 
a reduction of 5 to 15 per cent, being generally demonstrable at 
the end of twenty-four hours. 

The milder laxatives are often useful in the reduction of arterial 
tension. They act by depleting the portal system and by removing 
toxic materials which have irritant effects on the vascular walls 
and on the kidneys. The administration of ten grains of blue 
mass followed in six or eight hours by brisk saline purge is generally 
the most satisfactory method of treating the usual symptoms of 
hypertension such as headache, irritability, insomnia, palpitation, 
etc. 

Enteroclysis is often beneficial for similar reasons, especially in 
cases of colonic stasis. 

Sleep. — In many if not all cases blood-pressure falls during sleep 
(often 30 to 50 mm.) and is associated with a diminished peripheral 
pulse wave. 

Brooks and Carroll 2 found that night pressures were lower than 
day pressures in those who worked by day, whereas the condition 
was reversed in night workers. Pressure variations of from 7 to 
44 mm. were observed. The least amount of fall occurred in those 
with already low pressures. The maximum fall occurred about 
two hours after sleep began, the time at which insensibility is the 
greatest, and was followed by a gradual rise which attained its 
maximum in the afternoon. Getting out of bed entailed only a 

1 The intravenous injection of magnesium sulphate in cats leads to a sudden fall 
of pressure, and if the dosage is sufficiently large, to death. Ritter, Ueber d. Einfluss 
v. Salzlosungen auf den Blutdruck, etc., Deut. Arch. f. klin Med. Chir., 1910, 11. 
See also McNider and Mathews, Amer. Jour. Physiol., 1907, xx, 323. 

2 Proc. Assoc. Amer. Phys., 1912. 



304 TREATMENT OF ARTERIAL HYPERTENSION 

slight temporary rise without materially influencing the regular 
cycle. Frequent interruption of sleep tends to prevent the full 
measure and suddenness of the primary fall of tension. If the 
primary drop occurs before the patient wakes it does not recur the 
same night no matter how sound the sleep. The amount of noc- 
turnal urinary secretion is apparently independent of the fall of 
pressure. Prolongation of the sleep interval does not produce 
lower tension. Nocturnal sleep, or even absolute rest, causes an 
average slowing of the pulse rate of twenty per minute as long as 
compensation is good. 1 

Some cases of insomnia show a reversal of the normal pressure 
relations, i. e., a higher pressure by night than by day. When 
sleep is produced by paraldehyde the pressure is reduced to 10 mm. 
below the normal individual sleep level. 2 

The nitrites are sometimes efficient somnifacients in cases of 
arterial hypertension, which is evidence in favor of the fact that 
the fall of pressure is a factor in the production rather than the 
result of sleep. Most somnifacients owe their efficiency more to 
general nervous sedation than to depression of blood-pressure. 
The administration of bromides or chloral even in large doses does 
not increase the fall of pressure during sleep. Sleep may often be 
induced by warm baths, moist abdominal compresses, hot mustard 
foot baths, or gentle general massage administered two hours 
after the evening meal, which should be light in character. 

Insomnia is a frequent and troublesome symptom in hyperten- 
sive cases. Often it is the only symptom of which the patient 
complains. Successful results can only be obtained by a careful 
study of the individual case, but as a general rule the following 
factors should be eliminated or avoided: Concentrated mental 
work or strenuous physical exercise during the evening. Excite- 
ment of any kind whether by playing "Bridge" or otherwise. 
Excessive smoking or any coffee drinking after dinner. If 
strychnin or nux vomica is administered for therapeutic reasons 
the evening doses must be omitted. Business worries and house- 
hold cares must be laid aside. 

Rest. — Rest in bed for a week, with a milk diet is often the best 
remedy for reducing blood-pressure. It is likely that the mental 
relaxation thus brought about is more important than the physical 
repose. Gumprecht called attention to the fall of pressure observed 

» Klewitz, F., Der Puis im Schlaf, Deut. Arch. f. klin. Med., 1913, cxii, 3S. 
2 Bruce, Edin. Medico-Chir. Soc, June 6, 1900, p. 156. 



DIET 305 

in laborers on entering the hospital, a result which he attributed to 
the unwonted rest. But it is also a fact that patients who take 
their worries and anxieties to bed with them show less improvement 
than do those who submit to the ordeal and succeed for the time 
being in throwing all responsibilities overboard, leaving their 
intellectual realm bordering on a temporary nirvana. This is also 
strikingly exemplified by the patient whose symptoms all disappear 
the minute he leaves home for a vacation. 

Exercise.- — In ambulant cases of chronic arterial hypertension 
with good compensation the milder forms of exercise are of great 
benefit. Walking or golf are to be recommended, but with the 
warning that such exercise must be deliberate and that sudden, 
violent, or too prolonged efforts are harmful. The beneficial effects 
are attributable to a greater distribution of blood to the periphery, 
sudation, improved digestion and metabolism, as well as to the 
distraction and psychic relaxation thus induced. Severe or sudden 
exercise such as heavy lifting, running or stooping must be avoided. 
Patients should be cautioned against straining at stool. The 
writer has seen disastrous retinal hemorrhages result from lack of 
this precaution. Severe physical exertion in man may raise the 
blood-pressure from 110 to 180 mm., chiefly owing to the rise of 
intra-abdominal and intrathoracic pressure, 1 and. it is more than 
likely that where hypertension exists, even greater increments of 
pressure may occur. 

Diet. — Overeating. — The eating of food which has not been 
earned by physical exercise, is one of the greatest causes of arterial 
hypertension; hence the regulation of diet plays an important 
part in treatment. The chief indications are to restrict proteid 
food, especially meats, salt, and substances capable of causing 
renal irritation (condiments, alcohol) or digestive disturbance. 
The diet should be largely lactovegetarian, and limited in quantity 
so as to just supply the nutrient and caloric requirements. It is 
surprising on how small a ration metabolic equilibrium can be 
maintained in people past middle life. A high proteid ration, 
it is true, even with an increased amount of non-protein nitrogen 
in the blood, does not appear to directly influence blood-pressure, 
but there are certain types of nephritis in which it is harmful and 
certainly it must throw additional work on the kidneys. 2 Prolonged 

1 McCurdy, J. H., The Effect of Maximum Muscular Effect on Blood-pressure, 
Am. Jour. Physiol., 1901, v, 98. 

2 Frothingham and Smillie, "Different Nitrogenous Diets in Nephritis," Arch. 
Int. Med., 1915, xv, No. 2. 

20 



30(5 TREATMENT OF ARTERIAL HYPERTENSION 

fasting produces a gradual fall of blood-pressure which in Charteris's 
case amounted to 25 per cent, of the normal reading. The pressure 
returns rapidly to the normal after the resumption of food. 

In the case studied by Higgins in Benedict's 1 Laboratory, the 
general trend of both the systolic and the diastolic curves in both 
the sitting and in the prone posture was to decrease during the first 
fifteen days of the fast, systolic 134 to 94, diastolic 100 to 72 mm. 
Hg. This was followed by either a constant value or a slight 
tendency to rise during the last part of the fast. 

The decline of the blood-pressure is apparently due to: (1) a 
decreased contractibility of the heart muscle, and to (2) decreased 
vasomotor tone. The heart becomes smaller during the fast. Three 
days after the end of the fast, pressure was again normal. 

Thorough mastication and slow eating are essential. Neither 
mental nor physical exertion should be allowed immediately after 
food. Rest before eating often materially assists the subsequent 
digestion. 2 

Blood-pressure rises after the ingestion of food, probably as the 
result of gastric distention; this is followed by hypotension, which 
corresponds to the time of active gastric secretion, and finally 
there occurs a second rise which is probably due to intestinal 
distention and plethora, and which is proportional to these factors. 
It is evident, therefore, that large, bulky, stimulating meals should 
be avoided in arterial hypertension. 

In an uncooked state certain foods may exert a direct effect 
upon blood-pressure, perhaps due to their effect on the thyroid 
gland. Liver substance fed to rabbits causes a 50 per cent, increase 
in pressure, and, according to Lubarsch, vascular lesions; while 
the administration of taurocholate or glycocholate of sodium 
causes a fall. 3 

The question as to whether cardiac symptoms result from purely 
mechanical disturbances, such as alterations in blood-pressure, 
upward displacement of the diaphragm or heart, or from reflex 
action on the part of the vagus receives some elucidation from 
recent experiments. 

The abdomen is encircled by an inelastic bandage, and pressure 

1 Study of Prolonged Fasting, Pub. Carnegie Inst, of Washington, 1915, p. 119. 

2 The question of Diet has been reviewed and ably discussed by Hecht. Ueber 
d. diatetische Beeinflussung pathologischer Blutdrucksteigerung, Zeit. f. klin. Med. 
1912, lxxvi, 87. 

3 Van Leersum, E. C, Alimentare Blutdruckerhohung, Zeit. f. exp. Path. u. 
Ther., 1912, xi, 408. 



DIET 307 

(110 mm. Hg.) is exerted upon it by the inflation of a large rubber 
bag, observations on blood-pressure, together with radiographic 
studies of the diaphragm, being made. In health such a procedure 
produces a slight increase in the pulse and respiratory rate with a 
trifling fall of blood-pressure. In cardiopaths occasionally marked 
fluctuations of blood-pressure occur, but usually the results are 
closely akin to those produced in healthy people, showing that 
mere elevation of the diaphragm is of but little importance. Infla- 
tion of the stomach with air causes a slight fall, and with carbon 
dioxid, a rise of the diaphragm, chiefly of the left side. In health 
a slight rise of blood-pressure results from this procedure, in cardio- 
paths — especially in mitral disease — a marked fall of pressure (20 
mm.) occurs in about half of the cases, a fall which bears no relation 
to diaphragmatic displacement. 1 

It would seem, therefore, that gastric disturbances cause cardiac 
embarrassment chiefly through reflex and only secondarily through 
direct mechanical causes (see Tympanites, page 260). 

The main dietary rule is moderation. Meat in quantities up to 
100 or 150 gm. a day may generally be allowed. The prejudice 
against red meat and eggs is unfounded. There is chemically but 
little difference between red and white meats. If the amount be 
within the allowable limit it makes but little difference which the 
patient takes (see Nitrogen Retention, page 285). It is often neces- 
sary to restrict the use of sodium chloride, especially if the patient 
is edematous; for while there is no invariable absolute parallelism 
between salt retention and blood-pressure, the ingestion of salt in 
quantities greater than is demanded for physiologic equilibrium 
places unnecessary work on the kidneys. As a general rule, both 
the number and the bulk of meals is to be reduced, and extractives, 
soups, gravies, ate, are to be avoided. The use of fruits and 
vegetables, especially if cooked, and if they do not cause flatulence 
or other symptoms of indigestion, is to be encouraged . An absolutely 
salt-free diet is difficult to secure and excessively irksome to the 
patient, while the benefits derived from the same do not justify 
its adoption. Recent experiments indicate that the average in- 
dividual consumes much more salt than is necessary for physiologic- 
equilibrium. This combined with the use of condiments leads to 
greater consumption of both food and fluid than is required for 
nutrition, and thus throws an unnecessary work on the eliminative 

1 Funder, Ueber d. Einfluss intraabdominaler Drucksteigerung u. des Fullungszu- 
standes des Magens auf d. Blutdruck, Deutsch. med. Woch., 1913, xxxix, 646. 



308 TREATMENT OF ARTERIAL HYPERTENSION 

organs. Freshly made cheeses may be taken, but those which have 
been ripened must be avoided, since they contain oxyphenylethyl- 
amin, a bacterial decomposition product with marked pressor 
potency and identical with one of the toxic bases to which ergot 
owes its effects. 1 

Conservation of Energy. — In the early stages of increased blood- 
pressure the proper regulation of the daily life and diet is the only 
rational or efficacious method of treatment. The avoidance of 
hurry and worry are of prime importance, and are often the most 
difficult matters to correct. The patient should understand that 
the "doing of things against time," the doing of several things 
at once, the ceaseless mental concentration upon different problems, 
the assuming of unnecessary tasks and responsibilities, the frequent 
interruption of a train of thought by telephone calls, etc., are 
unwarranted drains upon vital energy, and that he who leads the 
high-pressure life is a physiologic spendthrift who is bound to end 
in early bankruptcy. This applies with special emphasis to that 
class of high-strung individuals who "go on their nerves," and 
who, as Holmes has said, "put energy out at interest and receive 
nervous derangement in return." "Worry, suspense, anxious 
anticipation, disappointment, consciousness of failure or of failing 
health, the hunted feeling that comes of overwork, and arrears, 
regret, sorrow, despair " — "wear out not only the nervous, but also 
the cardiovascular system." (Bruce.) 

Fluid. — Too much fluid throws an unnecessary burden on the 
kidneys. The old idea of flushing out the system, of diluting toxic 
products, etc., in patients already dropsical has been shown to be 
erroneous. The total intake in whatever form should in non- 
dropsical patients not exceed or fall below two liters per diem. 
A tumblerful of hot water flavored with lemon juice or rind, or 
with the addition of citrate of potassium, between meals and at 
bedtime is often beneficial. It is sometimes, although rarely, 
advisable to diminish the fluid intake even in cases free from 
dropsy. This should not be done if there is nitrogen retention in 
the blood. 

Hogan 2 has administered intravenously, saline solution containing 
sodium carbonate (20 gm. cryst., 2000 c.c.) in cases of high blood- 
pressure associated with uremia and believes that he produced a 

1 For literature see Edit. Am. Jour. Med. Sci., October 17, 1914. 

2 Alleged Danger of Intravenous Injections in High Blood-pressure, Lancet- 
Clinic, January 2, 1915. 



HYDROTHERAPY . 309 

marked fall of pressure, with sudation and symptomatic ameliora- 
tion. He explains this as due to the fact that if the concentration of 
the infusion is right, "the tissues and blood colloids are robbed 
of their water, and while tissue edema and high blood-pressure are 
decreased, free water is made available for excretion as urine, sweat 
and intestinal fluid." 

Alcohol is contra-indicated. In small well-diluted doses it may 
do no great harm, but when possible it should be eliminated entirely. 
The- use of tobacco should be restricted (see Tobacco and Blood- 
pressure, page 228). 

Hydrotherapy. — Warm baths are valuable depressor remedies, 
and an occasional Turkish or electric-light bath is often useful, 
although these procedures must never be prescribed without due 
consideration of the possible deleterious effects, i. e., marked 
temporary increase in blood-pressure before sweating occurs, 
vascular rupture, cardiac strain, and reduction of nervous tone. 
Saline baths (one pound of washing soda or sodium chloride to the 
tub) are more stimulating and produce more marked sudation. 
Navheim baths are especially useful if there be cardiac dilatation 
or weakness. A good sweat often causes a 10 to 20 mm. fall in 
pressure, which tends to last throughout the day, especially if the 
procedure be repeated daily. 

Occasionally, for reasons not yet understood, a series of sweats 
will reduce the pressure for weeks or months. This method of 
treatment is of course specially indicated if there be renal insuffi- 
ciency or threatened uremia, but the occasional employment of 
sweat-producing hydrotherapy is often advisable in the absence 
of these conditions. Just how it does good in uremia is uncertain. 
The amount of urea eliminated through the skin even with a copious 
sweat cannot exceed 10 or 15 grains, and it is improbable that other 
toxic products are thrown off in any greater proportions. The 
beneficial effects are probably brought about by a change in the 
mass movement and a redistribution of the blood, especially that 
in the splanchnic domain, the peripheral arterioles and capillaries 
being temporarily dilated and flushed with blood. According to 
Amblard, electric-light baths produce less primary rise in pressure, 
and are therefore to be preferred. 

After the sweat the patient should be allowed to cool off gradu- 
ally, being first wrapped in blankets, and after a time sponged 
or sprayed with cool water or alcohol. A sudden plunge in a cold 
pool or immersion under a cold shower bath, especially while the 



310 TREATMENT OF ARTERIAL HYPERTENSION 

patient is still actively perspiring, may produce an increase of 50 
mm. in blood-pressure, an occurrence which throws a tremendous 
strain on the cardiovascular system. 

It has been shown that the relative concentrating power of the 
skin and kidney for urea and ammonia are very different, though 
in each instance the values are higher than in the blood. 1 Further 
investigations may teach us that, depending upon the character 
of the toxin to be eliminated, sweat baths may be definitely indicated 
or contra-indicated in a given case. 

Hot Baths.— Baths of a temperature of 104° to 106° F. (40° to 41° 
C.) produce a primary rise of blood-pressure (vasoconstriction) 
with an increased pulse rate, followed by a temporary fall (vaso- 
dilatation) and finally a second rise (increased systolic output with 
increased pulse rate) which persists until exhaustion occurs. On 
terminating the bath the pressure falls below the normal. The 
systolic pressure is chiefly affected. Hot air, steam, and electric- 
light baths exercise effects proportional to their temperature. Hot 
baths must be employed with caution in the treatment of hyper- 
tension in diabetes. It has been shown that if the bodily tem- 
perature be raised either by fever or by artificial means the sugar 
content of the blood increases. 2 

Warm Baths. — Baths of a temperature between 99° and 101° F. 
(37° to 38° C.) generally lower blood-pressure, owing to a gradual 
primary vasodilatation, which is not, as in the case of hot baths, 
overbalanced by increased cardiac activity. 

Foot Baths. — Hot foot baths to which mustard may be advan- 
tageously added are often a satisfactory treatment for the headache 
and insomnia of hypertension. If the patient is to sleep the feet 
must be kept warm, and for this purpose a hot-water bag in bed 
is often desirable. 

Cold Baths. — The application of cold, especially in the form of 
forcible sprays and douches (mechanical stimuli), increases blood- 
pressure. The lower the temperature and the more sudden the 
application, the greater the rise. A sudden plunge into a cold pool, 
accompanied by the additional muscular efforts of swimming, 
produces a great increase in pressure, quite sufficient in arterio- 
sclerotic cases to cause vertigo and precordial oppression, to pre- 

1 Plaggemeyer, H. W., and Marshall, E. K., A Comparison of the Excretory Power 
of the Skin with that of the Kidney through a Study of Human Sweat. Arch. Int. 
Med., 1914, xiii, 159. 

2 Roily, F., and Oppermann, Das Verhalten des Blutzuckers b. Gesunden u. 
Kranken, Biochem. Zeitsch., 1913, xlvii, 187. 



COLD BATHS 



311 



cipitate an apoplexy, an attack of angina pectoris, or of pulmonary 
edema. 

In normal individuals the vascular reaction to heat and cold are 
general reactions, i. e., a cold bath reduces peripheral blood-flow 
and temperature, not only in the parts immersed but elsewhere. 
Even sitz baths have a similar effect, although the idea still persists 



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PULSE PRESSURE (AMPLITUDE) 

____ PULSE RATE 

- - BODILY TEMPERATURE C. 

Fig. 95.— Chart showing the effect of a tub bath of 41° C. (105.8° F.) upon the 
blood-pressure, pulse rate, and bodily temperature. The vertical lines indicate the 
beginning and end of the bath. (After Strassburger.) 



in some minds that blood is simply crowded out of the area to 
which the cold is applied and forced into other peripheral areas. 
This has been shown to be incorrect. In abnormal conditions, 
however, whether functional or organic in origin, local peripheral 
variations may occur. The peripheral application of cold produces 
cerebral hyperemia, whereas heat has the opposite effect. It 
also decreases systolic output, whereas hot baths increase the 



312 TREATMENT OF ARTERIAL HYPERTENSION 

latter. It should be remembered, however, that where sensory 
stimuli (friction, C0 2 , etc.) are added to the cold bath the systolic 
output may be increased despite the low temperature of the bath. 
Following a cold bath the reaction becomes reversed, the systolic 
output is increased and peripheral vascular dilatation occurs. 
When the circulatory apparatus is efficient or if the cold bath has 
been preceded by sweating, etc., the reversed reaction may set in 
even while the subject is still in the cold bath. The changes in 
blood-pressure which result from sensory or thermic stimuli are 
dependent both upon the state of the splanchnic veins and upon 
that of the peripheral arterioles. Blood-pressure may increase 
despite splanchnic dilatation as a result of peripheral contraction 
(cold baths, etc.), so long as the splanchnic vessels retain their 
tone. 

A cold bath is by far the most potent remedy which we possess 
for altering blood distribution. It adds, however, a distinct burden 
upon the heart. Spray and shower baths still further increase 
the burden by the sensory stimulation which they provoke. If 
the heart is weak, instead of a rise in pressure cold baths may 
actually cause a fall, because the heart weakens instead of responds 
to the call for increased effort. Indeed, syncope and sudden 
death may thus be precipitated. Nature, it appears, often wards 
off the latter events by rendering vasomotor nerves reactionless. 

O. Miiller has shown that not infrequently the peripheral 
arteries of cardiopaths are plethysmographically irresponsive to 
the local application of ice. It must be remembered, however, 
that although this may be true for minor reactions, such as those 
just mentioned, nevertheless a major reaction such as that produced 
by a cold bath may be suddenly fatal. With diseased arteries 
the sudden elevation of pressure which follows a cold bath may 
produce vascular rupture. 1 

Too frequent or too vigorous hydrotherapeutic measures tend to 
lower nerve tone and may do actual harm. In the thin, high-strung, 
hypertensive patient they must be used with caution. Too violent 
forcing down of the arterial pressure by means of baths, etc., is 
just as reprehensible as when the same end is attained by means of 
the nitrites. If the patient feels listless, weak, or exhausted, as a 
result of the baths, they are doing him harm, despite the fact that 
his pressure may be more nearly normal. Cold baths, although 

1 This subject has been admirably summarized by O. Miiller and E. Veiel, Samml. 
klin. Vortrage, 1909-10, N. F., 167-196 (innere medizin), p. 641. 



CARBONATED BRINE BATHS 313 

increasing the arterial, lower the capillary blood-pressure. The 
effect of hot baths upon the capillary pressure is less constant 
(Landerer) . 

Carbonated Brine Baths. — Despite the fact that Muller and Weiland 
have furnished plethysmographic evidences of peripheral vaso- 
constriction, and Liwschutz tachographic indications of an increased 
systolic output, it must be confessed that in a large number of 
cases treated with carbonated brine baths no constant pressure 
effects can be demonstrated. 

The pressure at the end of the bath or upon the completion of 
the treatment, in cases either of hypertension or of hypotension, is 
variable. On the whole, pressure is more frequently raised than 
lowered, but it is impossible to know beforehand in which way a 
given case may respond. 1 We do not mean to derogate the usefulness 
of this form of treatment, which is often followed by excellent 
results, especially in cases of cardiac weakness, but merely to point 
out that neither the subjective nor objective improvement rests 
on a basis of blood-pressure change. It is evident from the foregoing 
that such treatment must never be advised without due consider- 
ation. An increased pulse or systolic blood-pressure may be dis- 
tinctly harmful in a case of myocardial degeneration. Even less 
marked and less constant results are observed after the use of 
alternating current baths. 2 

The organism reacts to electric stimulation (faradic, galvanic 
or alternating currents) by a negative volume change as shown by 
the plethy sinograph. The effect upon the pulse rate and the blood- 
pressure is inconstant both in the same and in different individuals. 
Whether the benefits which sometimes follow electric baths in 
cardiac disease are due to cutaneous reflexes or to muscular con- 
traction is uncertain. 3 

Of course the effects of the baths depend largely on the tem- 
perature. If below 33° to 35° C. (92-95° F.) the pressure will be 
more apt to rise, if below this point, to fall. But with temperatures 
above 40° C. (104° F.) the pressure first rises and later falls. Hot 
and cold douches elevate and lukewarm douches lower tension. 
The effect on the pulse rate is equally important, heat accelerating 

1 Swan, J. M., The Influence of Carbonated Brine (Nauheim) Baths on Blood- 
pressure, Arch. Int. Med., 1912, x, 73. 

2 Laquer, A., Ueber d. Verhalten des Blutdruckes nach Kohlensaure u. Wechsel- 
strombadern, Zeit. f. exp. Path. u. Therap., 1909, vi, 855. 

3 Geissler, Der Einfluss Elektrischer Reize auf d. Blutvertheilung im Menschlichen 
Korper, Munch, med. Woch., 1908, lv, 92. 



314 TREATMENT OF ARTERIAL HYPERTENSION 

and cold retarding it. These effects are generally transient, not 
lasting more than an hour or two. 

Exception is often taken to the fact that carbon dioxid baths 
are used both in the treatment of arterial hypotension and hyper- 
tension. Their beneficial effects, which are unquestionable, are 
to be explained thus: The baths have essentially a cardiovascular 
tonic effect. Ordinarily they are followed by a rise in blood-pressure, 
an increased systolic output, and a slowing of the pulse. This 
leads to a generally improved circulation, nutrition, and excretion, 
and may indirectly lower blood-pressure, especially in cases of 
high-pressure stasis. Their action is thus comparable to that of 
digitalis. Those most competent of judging, state that these baths 
are harmful in cases of advanced renal lesions. This is probably 
due to the temperature (83° to 90° F.) to which the baths are 
lowered, for certainly the secretion of sweat and urine is distinctly 
increased in the average case to which this treatment is given. 

Cool carbon dioxid baths slow the heart and cause contraction 
of the peripheral arterioles. The thick layer of bubbles which 
surrounds the body in part prevents the loss of heat which occurs 
in ordinary cool baths, thus causing a pleasant sensation of warmth. 
Warm carbon dioxid baths increase the pulse volume, but have 
the opposite effect from cool baths upon the arterioles. Since 
these baths make considerable demands upon the circulation they 
must only be given under medical supervision. 

Oxygen Baths. — Oxygen baths have been extensively employed 
as a remedial measure in cases of arterial hypertension, and are 
said by numerous observers to be attended with very satisfactory 
results. A lowering of tension is more constant than in case of 
carbon dioxid baths. These baths are contra-indicated in the 
terminal hypotension of arteriosclerosis (Winternitz), 1 especially 
if associated with anemia (Baedeker). 2 

The baths which may be administered at home 3 are given at a 
temperature of 90° to 95° F., for from ten to twenty-five minutes. 
A course of baths (twenty-four) should be given on successive days, 
with occasional intermissions, either in the morning or at night 
(for insomnia), but not too soon after a meal. 

Phlebotomy. — Venesection is one of the most prompt and effica- 
cious methods of lowering blood-pressure and relieving a distended 

1 Blatter f. klin. hydrother., 1907, p. 1. 
s.Therap. d. Gegenwart, 1910, p. 2. 

3 "Perogen" baths. Morgenstern & Co.. New York. The oxygen is liberated by 
the admixture in the bath of two powders (sodium perborate and magnesium borate). 



HIGH-FREQUENCY CURRENTS 315 

right heart. Its beneficial effects in uremia are generally attributed 
to the foregoing effects and not to the amount of toxic material 
which is removed from the blood-stream. Phlebotomy is chiefly 
indicated in conditions of venous stasis, whether due to right or 
left ventricular weakness. It often yields excellent results in the 
treatment of acute pulmonary edema. In order to obtain definite 
results 300 to 500 c.c. of blood must be withdrawn. 1 A rapid 
venesection amounting to from 300 to 500 c.c. will generally reduce 
blood-pressure from 5 to 30 mm. As a rule the more rapid the 
withdrawal the more pronounced the fall of pressure. 

Bandaging of the Extremities. — The application of tourniquets to 
the extremities with sufficient constriction to prevent venous 
outflow, although allowing arterial inflow, has temporarily much 
the same effect upon the system as a phlebotomy. It may remove 
a 14-liter quantity of blood from the general circulation, and has 
been recommended as a method of treating heart weakness, but has 
not found much favor. If too much pressure is exerted, inhibition of 
arterial inflow and marked increase of general blood-pressure will 
result. The method must, of course, not be applied in the presence 
of edema or varicose veins of the extremities. Relaxation of the 
bandages must always be gradual so as not to suddenly increase 
cardiac work. By bandaging all four extremities, 20 per cent, of 
blood can be removed from the general circulation and the heart 
spared a corresponding amount of energy. Subjective symptoms 
are said to show a distinct amelioration. 2 This procedure has 
been useful in cases of threatened pulmonary edema and other 
conditions associated with increased venous pressure. Pronounced 
passive congestion in the extremities may cause a fall of 20 mm. 
Hg., sometimes rather suddenly, with signs of collapse. 

High-frequency Currents. 3 — Although there is as yet no unanimity 
of opinion on the subject, some very favorable reports have been 
published regarding the efficacy of high-frequency currents for the 
reduction of high arterial pressure. The current is said to act 
by lowering peripheral resistance and also by acting as a cardiac 
tonic. 



1 Moritz and Tabora, Verhandl. d. Kong. f. inn. Med., 1909, xxxvi, 378. 

2 Lillienstein, Der unblutige Aderlass, Phlebostase, Med. Klinik, 1912, vii, 316. 

3 Also spoken of as Arsonvalization after d'Arsonval, to whose physiologic studies 
so much of our present knowledge on the subject is due. For further information 
regarding the history, electric data, detailed description, and literature on this sub- 
ject see Allen, W. ('., Radiotherapy and Phototherapy, Philadelphia, 1904. Mann, 
L., Krause and Garre's Lehrbuch d. Therap. Inneren Krankheiten, 1911, i, 4SS, 509. 



316 TREATMENT OF ARTERIAL HYPERTENSION 

Nagelschmidt, 1 who reports good results in a series of 120 cases, 
believes that the discrepancies in the results attained by different 
observers with the high-frequency current are due to the fact that 
an insufficient amperage has generally been employed. 

The exact means by which high-frequency currents reduce blood- 
pressure are not thoroughly understood. The belief at present 
is that the effect is mainly thermal (local heating, rise of bodily 
temperature, and pulse rate, sudation and peripheral vasodila- 
tion) and that it is not due to cardiac depression. 

" If two electrodes from a galvanic or a faradic current are placed 
in a bowl of water, decomposition occurs with bubbles at either 
pole. Even if quite weak, a hand placed between them experiences 
painful electrolytic sensations. If these electrodes are replaced 
by high-frequency ones, hardly any electrolysis occurs. The water 
merely gets warm, and a hand placed between them experiences no 
sensation whatever excepting that of warmth, even with currents 
so strong that were they galvanic or faradic they would cause 
chemical and electrolytic changes capable of destroying the tissues" 
(Sayer). 2 

"With regard to alterations in the blood itself, we may look 
upon the action of high frequency in reducing blood-pressure as 
being in some way analogous to the action of a rise of temperature, 
when, unless there is dyspnea and cyanosis, the rapid metabolism 
caused by the onset of any fever is always accompanied by a fall 
in blood-pressure, an increased excretion of uric acid, and a quick 
capillary reflux, exactly what happens on a small scale with a dose 
of high frequency." 

The effect on the nervous system is definite, but the sensory and 
motor stimuli are too rapid to permit of a response, " for all electric 
vibrations beyond ten thousand per second lie beyond the limits 
of the range of frequencies to which these nerves can respond. 
Although no direct effects can be demonstrated, yet their applica- 
tion to any muscle or nerve does in some way affect it, for it is 
found afterward that its excitability to all ordinary electric (gal- 
vanic and faradic) stimulation is lessened" (Sayer). The high- 
frequency currents act specially upon the nerves of the vasomotor 
system, the splanchnics and the large sympathetic trunks, and 

1 Diathermic Treatment of Circulatory Disorders, Arch. Rontgen Ray, February, 
1912. 

2 The Effects of Electrical Currents upon Blood-pressure, British Med. Jour., 
October 8, 1910, p. 1052. 



HIGH-FREQUENCY CURRENTS 317 

the greatest effects are produced if the current is passed through 
these tissues. In nerves containing both constrictor and dilator 
fibers, ordinary electric stimulation produces a more marked effect, 
especially if weak currents are employed (Crilc 

Method of Application. — I. Induction. — The patient is placed 
in the centre of a wire cage, through the wires of which the current 
is passed. An induction current is thus generated in the patient. 

The presence of such a current can be demonstrated by means 
of an incandescent globe, held in the hand of the patient, which 
without any direct connection with the solenoid will become 
luminous (Mann) . 

II. Condensation. — "When the patient rests on an insulated couch 
or chair cushion, a high-frequency current derived from a static 
machine, or preferably from a specially designed apparatus, is 
passed through his body, using either a monopolar or a bipolar 
method (the patient being connected with the circuit by one or 
two pole electrodes, and acting as a current condenser). The 
strength of the current passing through the coil is gauged by an 
amperemeter, while the amount received by the patient can be 
gauged with a milliamperemeter placed between the table and the 
couch. Burch 1 has reported untoward results in some cases. He 
found that if patients who scarcely responded to from 20 to -50 
milliamperes were subjected to 200 to 800 milliamperes a very 
marked fall of pressure with signs of collapse sometimes occurred. 
Patients who readily respond to the smaller dose are, he believes, 
instances of spastic hypertension which can safely be treated 
with the heavier dosage. The cases that show no response to the 
milder current show the best results under the larger dosage. These 
cases are supposedly due to both a vasomotor spasm and a vascular 
degeneration with a relatively strong heart. 

III. Local Application. (Diathermic Method). — By means of 
electrodes of different kinds the current is conducted from a small 
solenoid to the patient. In order to insure greater penetration and 
to minimize the local effect which this mode of application chiefly 
favors, the current is taken from an alternating current generator 
and then interrupted by means of a jump-spark attachment. The 
action of this (diathermic) current is somewhat different from 
that of d'Arsonval (Mann). There is no cutaneous resistance. 
The current passes from one electrode to another by the shortest 

1 Electrical Treatment of Arterial Hypertension. Med. Record, 1911, Ixsx, S66. 



318 TREATMENT OF ARTERIAL HYPERTENSION 

route, permeating the intervening tissues with practically equal 
intensity. It is claimed that blood-pressure can be (1) raised, by 
precordiodorsal application, as the result of cardiac stimulation 
and cutaneous irritation, and (2) lowered, through peripheral 
dilatation, by application to the central nervous system (medulla). 
When one desires to heat the heart muscle itself, the large indifferent 
electrode is placed over the dorsal region, the smaller, movable 
one over the precordium. The latter must be so constructed that 
it is possible to pass 1000 to 1200 milliamperes for at least five 
minutes without undue heating of the skin (Nagelsehmidt). 

Indications. — High-frequency currents yield the best effects in 
cases of spastic hypertension with a relatively good heart muscle 
and kidneys. The effects produced are said to be more lasting 
than those resulting from the use of vasodilator drugs. They can 
lead to permanent benefit only when coupled with hygienic and 
dietetic correction. Too great a fall of pressure as the result of 
such therapeusis may, according to Moutier and Challamal, 1 be 
counteracted by the application of this current to the vertebral 
column. According to Fontana 2 the variable results obtained by 
high-frequency currents upon blood-pressure depend upon the 
permeability of the kidneys. The vascular dilation and increased 
metabolism which the current produces throws extra work on the 
kidneys which, if these organs are functionally active, causes a 
fall of blood-pressure, whereas insufficient kidneys fail to react 
and blood-pressure remains high. 

Massage. — Although the primary effect of massage, as the result 
of cutaneous stimulation, tends to raise blood-pressure, this effect 
is more than counterbalanced by its effect on lymphatic and venous 
flow. Good general massage, especially in association with Swedish 
movements, is one of the most useful measures which can be 
employed in the treatment of arterial hypertension. It supplies 
many of the benefits of exercise without the attendant expenditure 
of energy. 

Abdominal Massage. — Some authorities hold that this form of 
massage is contra-indicated in cases of hypertension and cardiac- 
disease. Experimentally in animals it increases blood-pressure, 
but some clinical observations show that this is by no means always 

1 De l'abaissement de la pression arterielle au dessous de la norniale par la d'arson- 
valization, Compt. rend. Acad. d. sci., Paris, 1905, cxl, 742. 

2 Dell'azione delle correnti ad alta frequenza sulla pussione arteriosa in rapporto 
alia permeabilita renale, Gazz. d. Ospedali e. d. Clin., 1914, xxxv, 523. 



PASSIVE EXERCISES 319 

the case. Indeed, a fall of pressure may be observed. Certainly 
compression of the large abdominal arteries tends to raise the 
general pressure at least temporarily, but generally (with judicious 
massage) this rise is slight and is soon more than counterbalanced 
by the good effect which the manipulations have upon digestion 
and intestinal peristalsis. 

When skilfully performed it has a generally sedative effect accom- 
panied by a slowing of the pulse and often a fall of blood-pressure, 
probably by its influence on local stasis in the mesenteric vessels, 
although vagus action may have a part in the results. 1 

Vibratory Massage. — This form of massage yields good results, 
requires less time, and does not necessitate undressing, but, as a 
therapeutic measure, it is less satisfactory than good general 
massage with passive movements. A valuable factor of the latter 
procedure lies in the hour's rest and relaxation which the patient 
should be instructed to take after its completion. Even prolonged 
vibration of the precordium is without effect upon the pulse rate, 
the blood-pressure, or the systolic output. 2 It has been claimed 
that definite blood-pressure-lowering effects can be obtained by 
concussion of the seventh cervical vertebra for a period of about 
five minutes, and that vibration of the sixth and seventh dorsal 
vertebrae tends, although less constantly, to increase vascular 
tension. 3 

Cutaneous Irritation. — Local irritation of the skin (mustard, 
capsicum, etc.) produces redness by dilatation of the capillaries 
and venules without a corresponding dilatation of the underlying 
arterioles. 4 Such methods of counterirritation find a distinct field 
of usefulness when applied to the feet, neck, or precordium in helping 
to relieve some symptoms of hypertension (insomnia, headache, 
precordial and epigastric oppression) as well as in mitigating the 
restlessness and delirium of acute infections, notably attacks of 
pneumonia. 

Passive Exercises. — This form of gymnastics administered either 
by an attendant or by machinery (Zander apparatus, etc.), since 
it supplies the beneficial effects of muscular exertion without an 
attendant expenditure of volitional nervous energy, tends to lower 

1 Ekgren, E., Ueber den Einfluss d. Abdom. Massage auf Blutdruck, Herzthatigkeit 
u. Puis, etc., Zeit. f. diatet. u physik. Therap., 1902, v, 191. 

2 Plate and Bornstein, Ueber d. Einfluss d. Herzvibration mit hoher frequenz 
auf d. Kreislauf, Ibid., 1913, xvii, 65. 

3 Abrams, A., Spondylotherapy, 1910, p. 248. 

J Wood and Weisman, Arch. Int. Med., September, 1912. 



320 TREATMENT OF ARTERIAL HYPERTENSION 

blood-pressure in a satisfactory manner, and is a useful adjunct 
to other forms of treatment. 

Climate. — A warm, equable climate is desirable. Winters may 
be spent in Egypt, Jamaica, Bermuda, Southern Califormia, etc. 
Moderate warmth and sunshine conduce to outdoor exercise which, 
when accompanied by gentle perspiration, is most desirable, but 
sudden chilling must be sedulously guarded against (see Altitude) . 

Psychic Treatment.— Certain types of high-pressure individuals 
are extremely susceptible to suggestion, and tend to become intro- 
spective. Cautionary advice in such instances must be tempered 
with encouragement. The additional element of self-worry must 
not be added to their other burdens. For this reason it is often 
inadvisable to tell the patient anything about pressure changes, 
particularly if these should happen to be for the worse. The 
beneficial effects of light exercise and diversions of different kinds 
owe much of their good effect to psychic impressions. 

Respiratory Gymnastics. — In certain cases of hypertension both 
symptomatic improvement and lowering of tension may be induced 
by breathing exercises. Space will not allow discussion in detail of 
the mechanism by which this is brought about; but such results 
are not difficult to understand when we consider that better aeration 
of the blood diminishes its centrally pressure-raising CO2 content. 
Proper action of the respiratory muscles, especially of the diaphragm, 
facilitates blood-flow to and from the heart, and increases venous 
and lymphatic flow in the digestive organs and elsewhere. Thus 
tissue metabolism and elimination are directly favored. 

That the question is not, however, a perfectly simple one is 
shown by Stewart's investigations, which proved that peripheral 
blood-flow (in the hands) was diminished by deep breathing. 

"The cause of the diminution in blood-flow produced by forced 
respiration is without question in part a mechanical effect on the 
action of the heart due to the changes in the intrathoracic pressure. 
Hill and Flack have stated that the left ventricle becomes smaller, 
as shown by Rontgen-ray pictures, the radial artery emptier, 
and the arterial blood-pressure lower with each forced thoracic 
inspiration. That a chemical change may also be concerned is 
indicated by experiments in the case of cyanosis already mentioned, 
in which oxygen inhalation distinctly increased the blood-flow 
in the hand without affecting the respiratory movements or the 
total pulmonary ventilation, while in normal persons it had no 
such effect. It mav be that the washing out of the carbon dioxid 



RADIO-ACTIVE SUBSTANCES 321 

by the forced respiration causes, even in such short experiments 

and with such moderate exaggeration of the respiratory movements, 
those changes in the distribution of the blood, particularly its 
accumulation in the great veins, which Henderson associates with 
'acapnia,' and which, according to him, are so important a factor 
in surgical shock. Other vascular changes — for example, a diminu- 
tion of the flow in the coronary circulation due to the fall of pressure 
in the aorta, which aid the mechanical changes in the thorax in 
decreasing the average output of the heart — may occur. Changes 
produced through the vasomotor centre on the peripheral vessels 
may also play a more direct part. This is at any rate suggested 
by the fact that the perceptible change in the flow caused by forced 
breathing is not the same for the two hands, as it might be expected 
to be were the whole effect a cardiac one. However, it is not 
intended to lay much stress on this suggestion, for the initial 
differences in the flow in the two hands are not sufficiently great 
to permit without hesitation the application of this criterion. The 
beneficial influence of oxygen on the flow in the case of cyanosis 
may be explained as the result of the oxygen action in diminishing 
the excitability to carbon dioxid of the vasomotor centre and other 
mechanisms affected by hypercapnia." 1 

Differential pressure in the lungs, breathing into rarefied air, 
has been used as a method of promoting blood-circulation. Bruns 
found that when the pressure of the air into which the patient 
breathes has been reduced to 8 to 10 c.c. H2O, both pulse and 
respiratory rate increase, peripheral flow as shown by the plethys- 
mograph, is increased and venous pressure falls. 2 

Radio-active Substances. — Our knowledge of the physiologic 
effects of radio-active substances is very meager. The employ- 
ment of these remedies is still in its experimental stage, and there 
is considerable evidence to show that the efficient therapeutic dose 
and the toxic dose are separated by but a narrow margin. 

The drinking of water charged with radium emanations appears 
to increase tissue metabolism, the activity of ferments and urinary 
flow. Good results attending its administration in cases of gout and 
of arterial hypertension have been reported. It is now generally 
believed that the beneficial effects obtained at certain health 

1 Stewart, G. N., Studies on the Circulation in Man, III. The Influence of Forced 
Breathing on the Blood-flow in the Hands, Amer. Jour. Physiol., 1911, xxviii, No. 3, 
p. 196. 

2 Bruns, O., Die kiinstliche Luftdruckerniedrigung u. d. Lungen, etc., Munch, 
mod. Woch., 1910, lvii, 2169. 

21 



322 TREATMENT OF ARTERIAL HYPERTENSION 

resorts such as Bad Gastein in the Austrian Tyrol, and Hot Springs, 
Arkansas, are due to the radio-active waters there present. 

Water charged with radium emanations, however, quickly loses 
its potency and hence bottled waters are inert. The artificial 
charging of water with radium emanations is now, however, possible, 
and favorable results may be obtained with home-charged water 
having a potency of 5000 to 20,000 Mache units when taken over 
prolonged periods of time. 

Solutions of thorium- X have been administered intravenously. 
Plesch, who employed this method of treatment in pernicious 
anemia, found a considerable lowering of blood-pressure associated 
with increased metabolism, oxygen consumption, and loss of weight. 

The action of vanadium on different organs and tissues is but 
little understood. It appears that the intravenous injection of 
this substance in mammals is but slightly toxic to the heart. It 
causes a rise of blood-pressure due to peripheral vasoconstriction, 
but repeated injections cause a fall of pressure due to fatigue of 
the vasomotor centre and the heart. The action of moderate doses 
upon the peripheral vessels is more marked than in the case of 
barium, and upon the splanchnic vessels, more marked than 
adrenalin. 1 

Prolonged application of the x-ray to the adrenals of dogs pro- 
duces well-marked structural degenerative changes in the glands. 2 
Zimmern and Cottenot 3 obtained a prolonged clinical fall of pressure 
(20-80 mm.), associated with subjective improvement, in sixteen 
cases of chronic hypertension. Quadrone reports somewhat similar 
results, but Groedel was unable to obtain any reduction in cases 
of hypertension by this means. 4 There is no rational basis for this 
form of treatment. The evidence at hand is not in favor of adrenali- 
nemia as a cause of chronic hypertension, and too prolonged ex- 
posure may do serious structural damage to the glands. 

The usual result of exposure in a radium emanatorvum is a fall 
of the systolic blood-pressure amounting to 20 or 25 mm. Hg. 
Together with this there generally occurs a decrease in cardiac 



1 Jackson, D. E., The Pharmacological Action of Vanadium, Jour. Pharm. and 
Exper. Therap., 1912, iii, 477. 

2 Cottenot, Mulow et Zimmern, Action des vagons sur la corticale sur renali, 
Compt. rend, hebdom. des sciences Soc. biol., 1912, lxxiii, 717. Similar results by 
Galansino and Decostello. 

3 Zimmern et Cottenot, La radiotherapie des glandes sur renales, ses resultats, 
ses effects hypotenseurs, Arch, d'electr., 1912, xx, 500. 

4 Groedel, F., Strahlentherapie II, 1913, p. 224. 



SURGICAL TREATMENT 323 

work and a lowering of the diastolic pressure. These changes are 
apparently due to vascular dilatation. 1 

Surgical Treatment. — Renal decapsulation has been performed in 
some cases of chronic nephritis. Goodman reports such a case 
in which both the systolic and the diastolic pressures were very 
definitely reduced for about two weeks following decapsulation, 
although the patient ultimately died. 2 

1 Loewy and Pleseh, quoted by Rowntree and Baetjcr, Radium in Internal Medi- 
cine, Jour. Amer. Med. Assoc, 1913, lxi, 1438. 

2 Goodman, E. H., Effect on Blood-pressure of Decapsulation of the Kidney, 
New York Med. Jour., October 3, 1914. 



CHAPTER XIV. 

EFFECTS OF DRUGS AND GLANDULAR EXTRACTS 

ON BLOOD-PRESSURE (ARRANGED 

ALPHABETICALLY). 

Aconite. — The effect of aconitin upon the mammalian heart 
may be divided into two phases: (1) It produces slowing of the rate 
with a weakening of contraction. The pulse rate may (experi- 
mentally) be reduced one-half and blood-pressure will fall propor- 
tionately. These phenomena are due to central stimulation of 
the pneumogastric nerve. (2) If the administration of the drug is 
pushed still further, tachycardia and arhythmia appear, apparently 
as a result of direct action upon the myocardium. 

Aconite has been used for the reduction of arterial hypertension, 
but its use has not been satisfactory. The tincture which is marketed 
without physiologic standardization varies greatly in potency, 
and in the doses usually employed is often inert. Robinson's 1 
investigations indicate that in maximal dosage aconite increased 
ventricular irritability. 

Alcohol. — There is much difference of opinion as to the clinical 
effects of alcohol on the circulation, and equally discordant findings 
have resulted from its employment experimentally. Most of the 
evidence shows that alcohol is only a momentary cardiac stimulant 
which acts reflexly through its irritation of the mouth, esophagus, 
and stomach. Its main effect is vasodilatation, and if pushed, 
nervous and muscular cardiac debility. If, therefore, temporary 
stimulation is desired it should be given in concentrated form; if 
vascular relaxation, diluted. Although it may briefly raise the 
systolic pressure it raises the diastolic pressure even more, and thus 
lowers the pulse pressure. 2 In chilliness due to peripheral vaso- 
constriction it does good, but if the patient be cold as the result 
of collapse, with a low blood-pressure, it is directly contra-indicated. 
It may act in part as a food by sparing the proteids or assist in 

1 An Investigation of the Potency of Tincture of Aconite, Arch. Int. Med., 1915, 
xv, Part I, 645. 

2 Lieb, C. C, Reflex Effects of Alcohol on the Circulation, Jour. Am. Med. Assn.. 
1915, Ixiv, 898, 



ATROPIN 325 

preventing acidosis, but in the vascular failure of infectious disease 
or in surgical shock it is harmful. It is irritant to the kidneys and 
delays the elimination of certain substances (uric acid, etc.). Both 
din ical and experimental evidence are against its use as a stimulant 
in conditions of low blood-pressure. 

It produces an unstable vascular tonus. Luzzato, on admin- 
istering 30 to 50 gm. of alcohol to students, found no constant 
relation between psychic phenomena, pulse or respiration and 
blood pressure. 1 Sphygmobolometric studies in fever cases gener- 
ally show a diminished amplitude, a lowered pressure, and decrease 
in cardiac work. 2 The onset of drunkenness is associated with a 
fall of the systolic and the pulse pressure, together with an increased 
pulse rate. 3 

The syndrome of cardiac dilatation with hypertension which is 
seen in excessive beer drinkers is in part due to the alcohol, in part 
to the increased volume of the blood. For obvious reasons alcohol 
should be taken sparingly if at all in cases of nephritic hypertension. 

Alkalies. — This class of drugs may indirectly assist in lowering 
tension by counteracting acid irritants, by combating dyspeptic 
tendencies or by their diuretic effect. 

Ammonium. — Ammonium in the form of the aromatic spirit is 
a promptly acting though temporary cardiac stimulant. It is 
useful in transient cardiac and vasomotor weakness, and extremely 
valuable in the relief of gaseous gastric distention in arteriosclerotic 
cases with precordial oppression. The following formula has often 
proved most satisfactory: 

1$ — Spts. ammonii aromat ttlxxx (2.0) 

Spts. chloroformi TUxv (1.0) 

Spts. lavendulse TUxxx (2.0) 

Aq. menth. piperita? ad f 3ij (8.0) 

To this prescription spirit of glonoin may sometimes be advan- 
tageously added. 

Atropin. — Atropin increases the pulse rate by depression of the 
peripheral ends of the vagus nerve. It has thus in part an antago- 
nistic action to digitalis. Experimentally it increases blood-pressure 
by a slight stimulation of the vasoconstrictor centre and an increased 

1 Luzzato, Accad. dei Fisiocritici di Siena, January 31, 1909. 

2 Dennig, Hindelang, and Grunbaum, Ueber d. Einfluss des alkohols auf d. Blut- 
druck u. d. Herzarbeit in path. Zustiinden namentlieh beim Fieber, Deut. Arch, 
f. klin. Med., 1909, xcvi, 153. 

3 Holzmann, Blutdruek bei Alkoholborauschten, Arch. f. Psychiatrie, 1909, xlv, 92. 



326 EFFECTS OF DRUGS ON BLOOD-PRESSURE 

pulse rate. Clinically, pressor effects are rarely demonstrable, 
although it is a valuable remedy in the wet, clammy stage of 
vascular collapse, in pulmonary edema (ha association with morphin), 
and in the treatment of hyperchlorhydria, which is a common 
symptom in cases of arterial hypertension. The following formula 
has often been prescribed with benefit for the last-named condition : 

1$ — Ext. belladonna gr. T V 

Pulv. rhei gr. \ 

Magnesii ustae grs. iv 

Carbo ligni gr. j 

To be taken in capsules or as a powder after meals. 

Caffein. — Caffein stimulates the entire nervous system, and 
may therefore be used if the circulatory disturbance is central in 
origin. 

Experimental Data. — Caffein injections in dogs cause a short 
rise (five seconds) followed by a fall of pressure (fifteen seconds). 
The larger the dose the greater the subsequent fall. 1 Caffein raises 
blood-pressure which has been depressed by alcohol, chloral, and 
infections even in late stages. Moderate dosage is more effective 
than large dosage, which latter deleteriously affects the heart. 
Caffein increases splanchnic tone. The experimental data are for 
the most part inapplicable to clinical work on account of the large 
dosage employed. 

The rise of pressure produced by caffein, which is never great, 
is due in part to increased splanchnic tonus and in the latter stages 
also to the increased pulse rate. Owing to splanchnic constriction 
the right heart receives more blood, and as the result of peripheral 
dilatation the outflow from the left heart is increased. Further- 
more, dilatation of the coronary arteries leads to better cardiac 
nutrition 2 and more forcible contraction. The pulse rate is usually 
not much affected, but retardation is more frequent than accelera- 
tion. 3 Large doses cause a fall of blood-pressure with diminished 
cardiac tonus. 

Caffein exerts a selective action on the vessels of the kidney. 
A primary constriction is followed by a marked secondary dilatation 
which, with a constant arterial pressure, causes a marked increase 
in local blood-flow and of urinary secretion. It is also believed to 
stimulate both the heart and the renal epithelium. Caffein is 

1 Pilcher, J. D., Jour. Phar. and Exp. Therap., 1912, iii, 609. 

2 Meyer and Gottlieb, Die Experim. Pharmacologic, Vienna, 1910, p. 263. 

3 Wood, H. C, Jr., Therap. Gaz., January 15, 1912. 



THE DIGITALIS GROUP 327 

capable of increasing urinary secretion even if a volumetric increase 
is prevented, probably as the result of increased blood-flow. 1 

Clinical Data. — The effect of caffein is more prompt and more 
brief than that of the digitalis group. It may be administered 
either in its pure form or as the citrate or in the form of tea or 
coffee. Medicinally it rarely produces a demonstrable rise of blood- 
pressure. It is useful as a cardiovascular and renal stimulant in 
both acute and chronic disease, but to be effectual must often be 
given in larger dosage than is customary. Better results are ob- 
tained by using theobromin-sodium salicylate, since the untoward 
effects of caffein are avoided. 2 

Camphor. — Camphor is said to raise blood-pressure by medullary 
and cardiac stimulation. The drug has long been used specially 
as a cardiac stimulant. Both clinically and experimentally it 
produces at least a temporary improvement of the pulse even in 
the agonal stage of infectious disease. It is normally neutralized 
in the body and thus rendered inert by glycuronic acid, and may 
produce toxic symptoms in cases in which the latter substance is 
diminished (starvation, cachexia, sepsis, eclampsia, CO2 poisoning). 
Nothing short of a toxic dose has any effect on blood-pressure 
in normal animals in health because compensatory vascular changes 
readily neutralize abnormal stimuli. Head and Brooks 3 failed to 
get any definite circulatory results either clinically or experimentally. 
The administration of the drug in emulsion has been commended 
as being a more certain and satisfactory method of obtaining the 
physiologic effects. 4 

The Digitalis Group. — Based purely upon experimental evidence 
digitalis should be the ideal drug to employ in case of arterial 
hypotension, since it increases the force of cardiac contraction as 
well as vascular tonus. Clinical data, however, show that in 
therapeutic dose digitalis often does not increase blood-pressure; 
in fact, it frequently lowers it, especially in heart diseases with high- 
pressure stasis and in hypertension due to toxic renal retention. 
Furthermore, its action is not sufficiently prompt for emergencies, 
and in febrile toxemias it often has very little if any effect, e. g., 
tuberculosis. So much experimental and clinical evidence has been 
amassed bearing on the subject of digitalis therapy as to forbid 

1 Weber, Arch. f. exp. Path. u. Phar., 1906, liv, 1. 

- Taylor, I., Clinical Studies in Caffein, Arch. Int. Med., 1914, xiv, 769. 

3 Aruer. Jour. Med. Sci., 1913, cxlv, 238 (bibliography). 

4 Doetoriwitch, Therap. d. Gegenwrt., xlvii, 343. 



328 EFFECTS OF DRUGS ON BLOOD-PRESSURE 

even a satisfactory summary. The good effects of this group of 
drugs cannot be ascribed essentially to an increased blood-pressure, 
and the belief that danger may attend its administration in 
conditions of high blood-pressure is equally unwarranted. For 
emergency use digitalis may be administered subcutaneously or 
intravenously. 1 H. C. Wood, Jr., believes that although medicinal 
doses of digitalis do not raise blood-pressure, yet they probably 
do have some slight effect on the vasomotor system. This view 
is based upon the fact that: (1) if slowing of the pulse is abolished 
by atropin, strophanthus causes a marked increase of pressure 
in normal man; (2) the diuretic effects of the drug, although inde- 
pendent of systemic pressure changes, may result from a relative 
splanchnic contraction at a time when the' renal vessels are dilated 
by the drug. 2 

Marvin, 3 in experiments on healthy students, found an increase 
in blood-pressure (average 13 mm.) which reached its maximum in 
five hours and gradually returned to the normal in fifty hours. 

Digitalis is often the most useful drug in cases of hypertension 
when the heart is beginning to fail. In such cases its use need not 
be feared on account of increasing vascular pressure. This effect 
is generally not in evidence, whereas it often lowers tension, espe- 
cially the diastolic pressure, by securing better elimination and a 
more efficient circulation. In auricular fibrillation digitalis does 
raise the average systolic pressure (see page 2-13). The action of 
digitalis and digitoxin is more prolonged than that of strophanthus 
and digitalin. 4 

In nephritic hypertension, as the renal lesion progresses, pressure 
continues to rise, and unless some other lethal termination occurs, 
either the heart or the vascular system must in time give way. 

Heart failure may manifest itself by (1) a fall of blood-pressure, 
edema, dyspnea, oliguria, and cardiac dilatation, or (2) high pressure 
stasis, a condition in which blood-pressure remains high or even 
rises (increased toxemia) and is associated with dyspnea, cardiac 
arhythmia and visceral stasis. 

In both these conditions digitalis is indicated. Under its ad- 
ministration renal elimination is increased and an actual lowering 

1 Digipuratum (extract of leaves), 0.1 gm. in twenty-four hours: Digalen, Tftxv 
(1 o.c), digitalin (German) gr. ^ to £ (0.002 to 0.015 gm.). 

2 Wood, H. C, Jr., Newer Ideas Concerning Digitalis, Therap. Gaz., June 15, 1915. 

3 Arch. Int. Med., 1913, xi, 41S. 

4 Hatcher, R. A., The Persistence of Action of the Digitalins, Arch. Int. Med., 
1912, x, 268. 



THE DIGITALIS GROUP 329 

of arterial pressure not infrequently seen. The final break can often 
be delayed by appropriate stimulation, for which purpose digitalis 
is by far the most satisfactory remedy. 

Digitalis exerts its effects on the kidney indirectly by its local 
effect on blood-flow; it also produces a direct local dilatation of 
the renal vessels. Its chief use in renal disease consists in its 
improvement of the local circulation by its effect upon the heart. 
It is the drug par excellence in cardiac insufficiency if the myo- 
cardium is still capable of response. Experimentally, ligation of 
the renal vein causes suppression of urine as well as ligation of 
the renal artery, showing that secretion is a question of blood-flow, 
not merely of blood-pressure, and digitalis not only increases 
arterial flow but diminishes venous stasis. When too freely 
administered, digitalis may cause centric voviiting. It has long 
been taught that emetics should not be given to arteriosclerotics 
lest the increased blood-pressure produced cause vascular rupture. 

From recent researches 1 it appears that vomiting is generally 
associated with a sudden and very great fall of pressure, due to 
cardiac inhibition but always associated with very great pressure 
variations. Great and sudden pressure oscillations may cause 
vascular damage at actual pressure heights which, had the rise been 
gradual would have been without serious effect. It is just as 
important, therefore, to avoid emesis in arteriosclerosis as was 
early taught, though for a somewhat different reason. 

Failing cardiac compensation is frequently associated with an 
increase of venous blood-pressure to or above 20 cm. Such a rise 
is therefore prognostically unfavorable, especially if it continues or 
increases despite the administration of digitalis or its congeners. 2 

Strophantkus and squills act in the same manner, but are less 
satisfactory than digitalis because of the variability of absorption 
of the former and because of the variability of activity and irri- 
tant (gastro-intestinal) qualities of the latter. In therapeutic 
dose neither strophanthin nor digalen affect the volume of the 
arm nor its normal reaction to the application of cold, although 
injections of these substances are said to affect the tonus of the 
larger arteries. 3 

1 Brooks, C, and Luckhardt, A. B., Blood-pressure during Vomiting, Am. Jour. 
Physiol., 1915, xxxvi, 104. 

2 Clark, A. H., The Diagnostic and Prognostic Significance of Venous Pressure 
Observations in Cardiac Disease, Arch. Int. Med., 1915, xvi, 587. 

3 Hewlett, A. W., The Circulation in the Arm of Man, Amcr. Jour. Med. Sci., 
1913, exlv, 656. 



330 EFFECTS OF DRUGS ON BLOOD-PRESSURE 

Depressants. — Chloral, the coal-tar group, bromides, etc. will, 
in sufficient dose lower blood-pressure. They should, however, 
never be used for this purpose, although they may on occasion be 
useful in relieving pain or promoting sleep. Chloral may produce 
degenerative changes in heart and liver similar to those following 
the administration of chloroform. 

Emetin. — This drug is sometimes administered intravenously. 
This is not a safe procedure, since the drug is a cardiac depressant. 
If this method of administration must be employed, coincident 
blood-pressure readings are desirable with a view to detecting 
evidences of circulatory failure (R. L. Levy). 

Epinephrin. — (See under Physiology, page 33). Epinephrin may 
be administered by mouth without any demonstrable cardio- 
vascular action. Prolonged use in this way leads to dyspepsia 
associated with colicky pains. Large doses given to rabbits produce 
arterial degeneration without increasing blood-pressure. 

Experimental Data. — Epinephrin produces upon the cardio- 
vascular system the same effect as would electric stimulation 
of the sympathetic — a marked rise of blood-pressure due to vaso- 
constriction and increased cardiac action (increased systolic output). 
This rise is of brief duration, due to fatigue. Venous pressure 
rises slightly. The different arteries are contracted in proportion 
to their sympathetic innervation. The coronary arteries are said 
to be unaffected (Schafer), owing to the absence of sympathetic 
fibers. In experimental animals epinephrin causes coronary 
dilatation, but in man (isolated arteries) and in monkey (perfused 
hearts) it causes coronary constriction, presumably because in the 
latter species the arteries are supplied with constrictor nerves 
of true sympathetic (thoracico-lumbar) origin. 1 Epinephrin dimin- 
ishes the pulse rate through vagus stimulation. 2 In small dose it 
increases the rapidity of the pulmonary circulation; in excessive 
dose it may cause pulmonary edema in men (Bennett) as it does in 
animals. Large doses and vagus stimulation diminish it. Apnea 
during artificial respiration has no effect on pulmonary circulation. 3 
The intraspinal injection of adrenalin causes a slower but more 

1 Barbour and Prince, Influence of Epinephrin on the Coronary Circulation of the 
Monkey, Jour. Exp. Med., 1915, xxi, 300. 

2 Meek and Eyster, Effect of Epinephrin on the Heart Rate, Am. Jour. Physiol., 
1915, xxxviii, No. 1. 

3 Langlois, P., and G. Desbouis, Sur la vitesse de la circulation pulmonaire. Adren- 
aline, Digitaliue, Asphyxie. Respiration Artificielle, Mem. 2, Journal de physiol. 
et de Pathol, gen., 1912, xiv, S. 1113-1123. 



EPINEPHR1N 331 

prolonged rise of pressure (40 mm. for half an hour or longer), 
although occasionally preceded by a primary fall (9 to 50 mm. 
for a half to four minutes). 1 

In using intraspinal injections care must be taken to avoid 
sudden increase of pressure. It is safer to allow inflow only by the 
force of gravity. Too high an intraspinal pressure is first mani- 
fested by cessation of respiration, soon followed by cardiac inhibi- 
tion and an enormous fall of blood-pressure. To combat cardiac 
failure under these circumstances, atropin is the most useful drug, 
whereas cocain is the best respiratory stimulant. Since the 
fall of pressure is not due to vasomotor failure, epinephrin is not 
indicated. The lowering of the intraspinal pressure after symptoms 
have arisen is unproductive of benefit. It has been suggested that 
a local hypodermic prophylactic injection of cocain and atropin be 
given at the site of the spinal injection, especially if the patient 
be under the effects of chloroform, since it not only minimizes the 
danger of sudden death but allows a larger injection to be given 
(Carter). 2 (See page 390.) Experimentally, epinephrin has by some 
investigators been found to be beneficial in hemorrhage, chloroform 
poisoning, pneumococcus septicemia, and diphtheria intoxication. 
On the other hand, Gottleib has shown that in rabbits receiving 
diphtheria toxin daily until cardiovascular symptoms appear, the 
injection of adrenalin only produces a brief and deceptive rise of 
arterial tension which soon leads to a fatal termination. 3 

Clinical Data. — A marked fall of blood-pressure due to vaso- 
motor depression without cardiac weakness is the chief indication 
of the use of epinephrin. Thus in shock, chloral poisoning, and 
collapse occurring in ether or chloroform narcosis it is decidedly 
useful. It should be administered intravenously in 5- to 10-minim 
doses (1 to 1000 solution) or, better still, in the proportions of 1 to 
50,000 as a continuous saline infusion. If a slower and more pro- 
longed action is desired it may be given subcutaneously, in which 
event its effects are usually manifest in from five to fifteen 
minutes. 

One naturally thinks of epinephrin in the vasomotor pareses 
of infections, but its use is under these circumstances disappointing. 
The condition here is not a sudden emergency with a good cardiac 

1 Auer and Meltzer, Proc. Soc. Exp. Biol, and Med., 1912, ix, 79. (Experiments 
on deeply narcotized apes). 

2 The Effect of Intraspinal Injections of Ringer's Solution in Different Amounts 
under Varying Pressures, Arch. Int. Med., 1912, x, 425. 

3 Gottleib, Arch. f. exp. Pharm., xxxviii and xliii. 



332 EFFECTS OF DRUGS ON BLOOD-PRESSURE ■ 

muscle, but a gradual failure of vasomotor and often cardiac 
strength. We must not forget that if the heart weakness is present 
a sudden increase of arterial pressure may be more of a load than 
the staggering organ can bear. The best and most lasting effects 
are obtained by slow intravenous administration in dilution with 
normal salt solution. Epinephrin has proved useful in vasomotor 
failure due to diphtheria, pneumonia, plague, peritonitis, and in 
surgical shock. 

Hypodermic epinephrin injections are variable in their effects. 
They do not always increase blood-pressure, but when they do so 
the rise generally lasts about one hour. The systolic phase is 
influenced more than the diastolic, indeed the latter may actually 
fall. Glycosuria may occur, but this bears no constant relation to 
pressure changes. A preliminary dose of atropin may increase 
the reaction even without increasing the heart rate. Marked 
reactions, both objective and subjective are often produced in 
cases of essential hypotension, whereas low pressure due to diarrhea 
and cachexia is but little influenced by epinephrin. In arterial 
hypertension marked reactions are sometimes obtained and caution 
must be observed. Epinephrin increases the demarcation of the 
sound phases as heard in the auscultatory estimation of blood- 
pressure (Clough). 

Ergot. — Experimental Data. — "The action of ergot may be shortly 
defined as a primary stimulation followed by paralysis (if given in 
large dose) of the motor terminations of the sympathetic nerve, 
which arises from the thoracic and lumbar spinal cord. The point 
at which ergot acts is thus analogous to that affected by adrenalin, 
but the range of ergot is more limited, for adrenalin affects not 
only the motor or positive nerve ends but also the inhibitory or 
negative fibers. In addition the effects of ergot are not so transitory 
as those of adrenalin, while, on the other hand, the latter does 
not exercise any subsequent paralyzing action of consequence" 
(Cushny). 

An intravenous injection of ergotoxin is followed by a prompt, 
abrupt rise of blood-pressure; this occurs after section of the 
splanchnic nerves, showing it to be a peripheral effect. The vessels 
of the abdomen and the extremities become contracted. The pulse 
rate is often increased at first, then diminished partly from vagus 
stimulation from high blood-pressure and partly from direct action 
upon the heart muscle. The rise of pressure varies greatly in 
different species (Cushny). The administration of a large dose 



ERGOT 333 

produces a secondary fall of arterial tension due to paralysis of 
the sympathetic fibers, which even epinephrin fails to overcome. 1 

Para-oxypkenylethylamin (isolated from ergot). — Experimentally 
this substance causes a rise of pressure due to capillary contraction 
associated with bradycardia and an increased pulse amplitude and 
diminution of blood in the veins. Its action is transient and 
followed by normal readings. 2 

Clinical Data. — Ergot is of very little if any use as a drug with 
which to restore vasomotor tone, its effects being very fugacious. 
Its action upon the pulmonary circulation has been discussed under 
Hemoptysis (see page 219). It is highly important that all ergot 
preparations used in medicine be physiologically standardized, 
not only because some preparations are inert but also because it 
has been shown that ergot sometimes contains small amounts 
of acetylcholin which has been pronounced to be the most powerful 
circulatory depressant known, as small an amount as one-millionth 
part of a milligram causing a fall of blood-pressure in rabbits. 3 

Hydrastis. — Although rarely employed in medicine, hydrastis is 
occasionally recommended in the treatment of hemoptysis owing 
to a supposed vasoconstrictor action. Experimental evidence, 
however, indicates that it has no such effect. W. W. Williams, 4 
from a careful experimental research, comes to the following 
conclusions: 

The most constant and conspicuous effect of the intravenous 
injection of hydrastis is a prompt fall of blood-pressure. With 
small doses the pressure promptly returns to normal, and there 
may be a slight rise above normal. With larger doses (from 0.07 c.c. 
to 1 c.c. per kilogram of body weight) there is only partial recovery 
from the fall of blood-pressure, or it may remain low. The pressure 
phenomena are attributable to depression of the cardiac muscle, 
causing the fall, and to stimulation of the muscle, causing the rise. 
Very large doses depress and paralyze the vagus and vasomotor 
system; otherwise there is no evidence deduced from the myo- 
cardiograms and oncometer that the vasomotor system has any 
important part in the blood-pressure changes. 

The two principal alkaloids of hydrastis, hydrastin and berberin, 

1 Dale, Jour. Physiol., 1906, xxxiv, 163. 

2 Bickel, A., and Pawlow, M., Untersuchungen z. pharm. Wirkung des p. Oxy- 
phenylaethylamins, Biochem. Zeitsch., 1912, xivii, 345. 

3 Editorial, Jour. Am. Med. Assn., 1914, lxiii, 2136. Discussion and literature. 

4 The Effects of Hydrastis and its Alkaloids on Blood-pressure, Jour. Am. Med. 
Assn., January 4, 1908, p. 26 (bibliography). 



334 EFFECTS OF DRUGS ON BLOOD-PRESSURE 

cause qualitatively the same blood-pressure changes, although 
berberin is the more active and is responsible for about 85 per cent, 
of the effect of hydrastis — hydrastin causing the remaining 15 per 
cent. Hydrastis given by mouth or hypodermically causes no 
change in the blood-pressure, heart rate, or respiration. 

Hydrastinin, an artificial alkaloid, derived from hydrastin, causes 
a rise of blood-pressure above normal, which is usually preceded by 
a slight fall when injected intravenously. The rise is well sustained 
and is principally caused by stimulation of the cardiac muscle. 

;, The results of this investigation do not support the clinical 
theories concerning hydrastis. It is possible that conditions in 
man and in disease may modify the actions observed by me, but 
this is rather improbable. At least the uniform contradiction of 
the experimental results and clinical opinions demands that the 
latter be examined critically before they are accepted." 

Hormonal. — This drug has been used as a remedy against intes- 
tinal atony and paralysis. Mohr states that his experimental 
research on hormonal has established beyond question its pro- 
nounced effect in reducing blood-pressure even with doses propor- 
tionately far below those used in the clinic to date. He had an 
experience with a threatened collapse in a man, aged twenty- 
eight years, after intravenous injection of 14 c.c. of hormonal, and 
since then, he says, four similar cases have been reported. Madlener 
has recently reported the death of a patient after injection of 20 c.c. 
hormonal for paralytic ileus following a myoma operation. Saba- 
towski's research on dogs has further confirmed the sudden pro- 
nounced drop in the blood-pressure after intravenous injection of 
hormonal. 

The Iodids. — Regarding the effect of the iodids on blood- 
pressure there is a difference of opinion. Certainly they are not 
active vasodilators in the sense that the nitrites are. On the other 
hand, cases are occasionally encountered in which a lowering of 
tension occurs, a response which naturally suggests that the hyper- 
tension was reflexly due to syphilitic aortitis or directly to endar- 
teritis. The former may exert an effect on the depressor nerve, 
the latter may cause loss of vascular elasticity from cellular 
infiltration. 

Numerous explanations for the physiologic effect of the iodids 
have been offered: (1) germicidal action; (2) increase of opsonins; 
(3) leukocytosis and increased lymphatic flow; (4) specific action 
of free iodin on gummatous tissues; (5) increased vascular perme- 



THE IODIDS 335 

ability; (0) stimulation of the thyroid gland; (7) the formation of 
a proteolytic ferment (Dick); (8) decreased hemic viscosity. Of 
these the last three chiefly merit consideration. 

Decreased viscosity undoubtedly occurs, but, according to 
Determann, 1 not in excess of normal physiologic variation. Capps 2 
has in a recent excellent review favored the theory of proteolysis, 
due to a ferment which has a selective although not specific action 
"on diseased granulomatous tissue of the arteries in a certain 
group of diseases," there being evidence to show that the iodids 
may exert such an effect in tuberculosis, actinomycosis, and leprosy. 
Such a ferment is assumed to result from the union of the iodid 
with the antibodies of the infected invididual. 

Experimentally, potassium iodid, if administered intravenously 
causes a fall of blood-pressure, but it has been shown that this 
effect is solely due to the effect of the kation (potassium) while the 
action of the ion (iodid) is actually one of stimulation, both of heart 
and bloodvessels. 3 A number of organic iodin preparations have been 
placed on the market with the claim of lessened gastro-intestinal 
irritation, absence of iodism, ready absorption, etc. Excepting 
preparations of the thyroid gland, they have no specific action other 
than that of iodin. The iodized proteins cause less gastric irri- 
tation; the more stable compounds are not entirely split in the 
body, and, therefore, not well utilized, while the less stable ones 
have no advantage over the alkaline iodids. Iodized fats and fatty 
acids are more slowly and evenly split, so that the amount of avail- 
able iodin in the blood varies less than when the alkaline iodids are 
used. The diminished frequency of iodism seems to result from the 
difference in the available iodin present in the body at a given time. 4 

The absorption of iodids from the intestinal tract is rapid up to 
a certain point, beyond which a stoppage occurs which apparently 
results from some local action. It is unaffected by blood-pressure 
except when this is very low, when absorption is somewhat slower. 5 

Summary. — So far as hypotensive effects are concerned the iodids 
may be employed in syphilitic arteritis and in lead poisoning, q. v. 

1 Das Verhalten d. Blutviskositat bei Ioddarreiehung, Deut. med. Woch., 1908, 
No. 20. 

2 Effects of Iodids on the Circulation and Bloodvessels in Arteriosclerosis, Jour. 
Am. Med. Assn., October 12, 1912, p. 1350. 

3 Macht, D. I., Action of Potassium and Sodium Iodids and of Iodin Ion on the 
Heart and Bloodvessels, Bull. Johns Hopkins Hosp., September, 1914. 

4 McLean, F. C, Organic Iodin Preparations, Their Pharmacologic and Thera- 
peutic Value, Arch. Int. Med., 1912, x, 505. 

5 Hanzlik, P. J., Quantitative Studies on the Gastro-intestinal Absorption of 
Drugs, Jour. Pharm. and Exp. Therap., 1912, iii, No. 4. 



336 EFFECTS OF DRUGS ON BLOOD-PRESSURE 

The custom of giving small doses over prolonged periods of time in 
other varieties of hypertension, while very common, is probably 
useless. The iodids have no direct effect upon blood-pressure. 

Mistletoe (Viscum Album). — Mistletoe has been used, chiefly 
in Europe, for the purpose of lowering blood-pressure. Experi- 
mentally (in a dog) intravenous injection promptly and progres- 
sively lowers blood-pressure 20 or 30 mm. Hg. This is associated 
with acceleration of the pulse, with diminished amplitude, and 
after a stationary period, a gradual rise of pressure to the normal 
level (one to two hours) . This action is the result of central depres- 
sion of the vasomotor centre. 1 Mistletoe has been given in doses of 
30 to 60 m. of the fluidextract. 

The Nitrite Group. — The most potent, as well as the most mal- 
administered and abused of the blood-pressure-lowering remedies are 
the nitrites. Their action is rapid and their effect is for the most 
part fugacious. Furthermore, a tolerance for this class of drugs 
is rapidly established (Fig. 96) . They should therefore be given fre- 
quently and in sufficient dose to produce their physiologic effect. 
The typical action is not only vasodilatation but also an increased 
systolic output which occasions a more rapid flow. 2 The following 
table shows the effect of these drugs upon normal individuals: 

Table I. — Average Blood-pressure Results from Administration of 

Nitroglycerin, Sodium Nitrite, and Erythrol Tetranitrate to 

Normal Persons. (AVallace and Ringer.) 



Time of 


Time of 


Time of 


Maximum 




beginning 


maximum 


duration of 


extent of 




action. 


effect. 


action. 


action. 




Drug. Min. 


Min. 


Min. 


Mm. Hg. 


Per cent. 


Amy] nitrite, 3 minims . 1 


3 


7 


15 


11 


Nitroglycerin, if minims, 










1 per cent. sol. ... 2 


8 


30 


15 


11 


Sodium nitrite, 1 gr. . . 10 


25 


00 


14 


13 


Erythrol tetranitrate, \ gr. 15 


32 


120 to 240 


16 


14 



It will be noted that promptness of action and duration of the 
effect tend to vary inversely. The therapeutic effects are obtained 
about as promptly when the drug is given by mouth as when it is 
administered hypodermically. The percentage of fall is markedly 
uniform, the higher the initial pressure the greater the drop. 

Physiologic Action. — Different members of the nitrite group of 
drugs have an essentially similar action. Their effects vary only 
in promptness, intensity, and duration." The chief action of the 

1 Gaulthier, R., Etudes physiologiques sur le qui, Arch. Internat. d. pharmaco- 
dynamic, 1910, Nos. 1 and 2. 

2 Cameron and Hewlett, Jour. Med. Research, December, 1906. 



THE NITRITE GROUP 337 

nitrites is that of lowering blood-pressure (depression of the nerve 
endings and musculature of the arterioles) and acceleration of 
the pulse rate, thus causing an increased rate of blood-flow. The 
veins are also dilated. The vessels most affected are those of the 
splanchnic system and of the head. 
Mode of Action. — Nitroglycerin is represented by the formula: 

CH2ONO2 

I 

CHONO2 
I 
CH2ONO2 

"It is probable, however, that in the presence of water and 
hydrochloric acid in the stomach it is decomposed, and that its 
decomposition products N0 2 and NO are disengaged in the form 
of brown vapors which are irritants and strong oxidizers. These 
ultimately produce an impression on the centripetal nerve endings 
in the gastric mucosa, which impulse is carried to the vasomotor 
centre and by the centrifugal nerves conveyed from the centre 
of the vascular wall, thereby causing the expansion of the vessels. 
This dilatation is due either to inhibition of the vasoconstrictors 
or to stimulation of the vasodilators" (W. H. Porter). 1 

Not infrequently patients exhibit marked idiosyncrasies to the 
nitrites: some bear them very badly and are much more affected 
by one member of the nitrite group than by another; others can 
take enormous doses (one grain of nitroglycerin daily has been 
given with apparent benefit). The administration of the nitrites 
coincidently with digitalis is a therapeutic blunder. The effect of 
the former will have passed off long before that of the latter has 
begun to act. Nitroglycerin has a retarding effect on renal secretion 
(Loeb) . Nitrite of amyl acts primarily upon the cerebral vessels — 
more so than the other nitrites. 

Table II. — Avebage Blood-pressure Results from Administration of 

NlTBOGLYCEBIN, SODIUM NlTBITE, AND EbYTHBOL TeTBANITRATE TO 

Patients with Aeteeiosclerosis. (Wallace and Ringer.) 2 





Time of 


Time of 


Time of 


Minimum 






beginning 


maximum 


duration 


extent of 






action. 


effect. 


of action. 


action. 




Drug. 


Min. 


Min. 


Min. 


Mm. Hg. 


Per cent 


Nitroglycerin, jq gr. 


. . 2 


8 


35 


32 


17 


Sodium nitrite, 2 gr. 


. . 15 


45 


120 


53 


25 



Erythrol tetranitrate, 2 gr. 30 60 180 60 30 

1 Jour. Am. Med. Assn., August 3, 1912. 

2 The Lowering of Blood-pressure by the Nitrite Group, Jour. Am. Med. Assn. 
1909, liii, 1630. 

22 



338 EFFECTS OF DRUGS ON BLOOD-PRESSURE 

In hypertensive cases the response is sometimes less prompt 
(delayed absorption) and the action more prolonged (delayed excre- 
tion) . The percentage fall is much the same in both tables. Head- 
ache is less frequent in high-pressure cases; indeed, it is often 
relieved by these drugs. 

The employment of the nitrites in hypertension is purely symp- 
tomatic medication. It temporarily relieves high pressure as certain 
forms of headache are relieved by acetanilid. It does not affect 
the underlying cause, and if used indiscriminately may do actual 
harm. The nitrites are often given in too small doses and too 
infrequently, especially since toleration is rapidly established; 
sV grain of nitroglycerin is often a better dose than twq, and as 
high as Yft may be given in emergencies. 

The nitrites are essentially emergency drugs to be given in case 
of a threatened apoplexy or cardiac failure from hypertension, 
etc. The splanchnic dilatation relieves the systemic, especially the 
intracranial pressure, but, of course, after intracerebral vascular 
rupture has occurred the nitrites are contra-indicated. Many 
preparations on the market are inert. The dosage must be based 
on the physiologic effect, flushing, headache, and a fall of pressure. 
Nitroglycerin is also used as a therapeutic test agent to determine 
whether certain symptoms are due to spastic vascular contraction. 
It is contra-indicated in arterial hypotension, and should therefore 
not be used as a primary cardiac stimulant in acute febrile disease 
or shock. 

Form of Administration. — Nitrite of amyl, in glass capsules (to 
be kept in the dark), to be crushed in a handkerchief and inhaled. 
The primary fall of pressure is followed by a rise to above the original 
level (Hewlett) . In cases of cardiac weakness, instead of a secondary 
rise of 6 to 10 mm., a fall of pressure occurs (Abrams) . 

Nitroglycerin, preferably as a 1 per cent, solution (spiritus 
glycerylis nitratis), to be swallowed, or as tablets to be dissolved 
on the tongue. Dose tto to tV grain. 

Sodium Nitrite. — Tablets to be swallowed or dissolved on the 
tongue. Dose: gr. ss to gr. ij (solutions deteriorate rapidly). 

Erythrol Tetranitrate. — Tablets. Dose: gr. \ to gr. ss. Erythrol 
tetranitrate produces the most severe headaches. 

Mannitol nitrate (gr. j) ; effect even more prolonged than erythrol. 

On the whole the spiritus glycerylis nitratis is the best prepa- 
ration, both because of its reliability and because of the ease 
with which the dose can be increased. 



OPIUM 



339 



If a prolonged and gradual effect is desired the nitrites should 
be given after meals. If taken between meals the drug should be 
well diluted. Sudden effects are generally as useless as they are 
undesirable. 

Summary. — 1. "The general indications for the use of nitro- 
glycerin are (a) to relieve symptoms of localized arteriosclerosis 
or arterial spasm in vitally important regions of the body and 
when there is pain due to contracted or diseased arteries in other 
regions; (b) to reduce general high blood-pressure in selected 
cases, if its continuance threatens accidents to the cardiovascular 
apparatus; and (c) to clear the diagnosis (see p. 300). 

2. The chief contra-indications to the use of nitroglycerin are 
(a) low or relatively low blood-pressure; (b) advanced chronic 
nephritis with very high blood-pressure and toxemic conditions 
producing high blood -pressure, as a rule; and (c) the presence of 
an idiosyncrasy in regard to its action." 1 



MINUTES 
1 15 30 




LIQUOR 
TRINITRINI 



\SODIUM lERYTHROL MANNITOL 

NITRATE TETRANITRATE NITRATE 



Fig. 96. — Diagram showing the comparative promptness of action and duration of 
effect of different blood-pressure-lowering drugs. (After Mathews.) 

Opium. — In some cases of hypertension (angina pectoris, broken 
compensation, etc.) morjrfrin is an indispensable drug. It often 
produces a most satisfactory fall of pressure as well as relief from 
symptoms, the former being doubtless largely due to its general 
sedative influence on the nervous system and its stimulation of the 
vagus nerve. Under its influence the cyanotic skin is often replaced 
by a pink flush indicating a dilatation of the peripheral circulation. 
The danger of this drug in nephritis has been greatly overestimated. 
The beneficial effects of opium are also in part due to its effect on 
the respiration. Edsall has shown that superficial rapid respira- 
tions such as are seen in cardiac dyspnea, etc., are functionally 
less efficient than slower labored movements. 2 It tends to lower 



1 Cornwell, E. E., When and How to Use Nitroglycerin, Jour. Am. Med. Assn., 
1913, lxi, 118. 

2 Edsall, D. L., The Efficiency and Significance of Different Forms of Respiration, 
Trans. Assoc. Amer. Phys., 1912, xxvii, 560. 



340 EFFECTS OF DRUGS ON BLOOD-PRESSURE 

blood-pressure by central vagal slowing of the pulse. 1 In the case 
of normal hearts during nocturnal sleep the pulse rate is slowed 
about twenty beats per minute, and although the slowing thus 
produced becomes progressively less, the worse the cardiac com- 
pensation, yet notwithstanding the establishment of sleep, induces 
very considerable cardiac rest. 2 Morphin produces a mild, codein 
only a slight, dilatation of the coronary arteries. Narcotin and 
papaverin cause marked dilatation. But morphin and narcotin 
combined have less effect than either separately. A combination 
of caffein (which of itself produces coronary dilatation) with papa- 
verin causes dilatation of the coronary ring. 3 

Pilocarpin. — Is a powerful diaphoretic, the physiologic action of 
which is directly opposite to that of atropin. Full doses slow the 
cardiac rate and diminish contraction through vagus stimulation. 
Still larger doses depress the heart muscle directly. Toxic doses 
cause peripheral vasodilatation by depressing the vasoconstrictor 
centre. It therefore tends to lower blood-pressure. 

It has long been used as a diaphoretic in renal disease, especially 
in conjunction with hot packs or hot-air baths if the patient does 
not sweat sufficiently from the latter procedures alone. It must, 
however, be given with caution in cases of heart weakness, since 
it may produce pulmonary edema. This accident can, however, 
be promptly corrected, if treated in time by full doses of atropin 
(gr. 5V hypodermically) . The usual dose of pilocarpin for adults 
subcutaneously is tV grain (0.006). 

It has been recommended in small doses (gr. 3V) thrice daily in 
water after meals to relieve arterial hypertension and its associated 
symptoms, especially headache. 4 

Pituitary Extract. — This substance has a more prolonged though 
less marked blood-pressure raising effect than epinephrin. Too 
frequently repeated it depresses respiration. It also has a diuretic- 
effect due to direct stimulation of the renal cells, usually aided 
probably by a concomitant vasodilatation, because there is no con- 
stant relation between pituitrin diuresis and either systolic or pulse 
pressure or the ratio between them. As a general rule, however, 

1 Van Egmond, Die Wirkung des Morphins auf d. Herz, Arch. f. exp. Path., 
1911, Ixv, 197. 

2 Klewitz, F., Der Puis im Schlaf, Deut. Arch. f. klin. Med., 1913, cxii, 38. 

3 Macht, D. I., Action of the Opium Alkaloids, Jour. Am. Med. Assn., 1915, lxiv, 
1489. 

4 Robinson, W. D., Pilocarpin in High Blood-pressure, Trans. Am. Climat. Assn., 
1914, xxx, 290. 



SALVARSAN 341 

it is accompanied by a decreased pulse pressure. 1 Furthermore, 
there is no constant relationship between renal volume and pituitary 
diuresis, 2 with local renal vasodilatation. 3 It stimulates the heart. 
It may be given hypodermically, intravenously, or by mouth. 
It may be used instead of epinephrin in cases of temporary hypo- 
tension or in cases of pulmonary hemorrhage, q. v. It causes con- 
traction of the peripheral arterioles, increases cadiac contraction, 
and slows the pulse. These results are due to a direct effect upon 
the cardiac and arterial musculature. It has been recommended in 
all cases in which lowered blood-pressure is due to loss of splanch- 
nic vascular tone, and in hypotension due to shock or toxemia, 
especially in combination with saline infusion. 4 Musser 5 Jr., 
who administered pituitary extract by mouth (0.065 dried gland, 
q. d.) obtained very constantly a distinct elevation of blood-pressure 
(up to 28 mm. Hg.) which often persisted for a time after dis- 
continuance of the drug. Diarrhea was sometimes produced. 
Commercial preparations of the posterior lobe vary greatly in 
potency, and should be standardized, Roth suggests, by their action 
on the isolated uterus of the virgin guinea-pig. 

Spartein. — Spartein sulphate stimulates the vagal ganglia and 
depresses the heart muscle. It slightly stimulates the ganglia of the 
vasoconstrictor nerves but clinically produces no demonstrable 
rise of blood-pressure. 

Strophanthus. — The action of this drug is essentially that of 
digitalis. Its effects are somewhat less lasting, perhaps because, 
as suggested by Eggleston, it is less firmly fixed in the tissues and 
more promptly eliminated. If used, it should be given intraven- 
ously in the form of strophanthin. 6 Its absorption from the gastro- 
intestinal tract is variable and uncertain (Hatcher) . 

Salvarsan. — Experimentally, small doses produce but slight and 
temporary effects on blood-pressure. Moderate doses cause a slight 
fall at the end of two minutes, a secondary rise and a tertiary 
decline (two to six minutes) . Large doses lower pressure at once. 

1 Hoskins and Means, Relation of Vascular Conditions to Pituitrin Diuresis, 
Jour. Phar. and Exper. Therap., 1913, iv, No. 5. 

2 Schaeffer and Herring, Philos. Trans. Royal Soc, Sect. B, 1908, cxcix, 1. 

3 King and Stoland, Am. Jour. Physiol., 1913, xxxii, 405. 

4 Klotz, Internat. Congr. Physiotherapy, Berlin, 1913. 

6 Effects of Continuous Administration of the Pituitary Gland, Am. Jour. Med. Sci., 
1913, cxlvi, 208. 

6 Subcutaneous dose: cryst. strophanthin, gr. T §„ (0.0005 gram), once in twenty- 
four hours. Intravenously in 1 to 6000 saline solution of strophanthin (Boehringer), 
gr. rjti t° Zo (0.0005 to 0.001 gram). 



342 EFFECTS OF DRUGS ON BLOOD-PRESSURE 

Both alkaline and acid solutions of salvarsan experimentally cause 
a fall of blood-pressure. If an excess of alkali is added blood- 
pressure may rise but this is purely due to the alkali which has 
physiologically overantagonized the salvarsan. Cardiac dilatation 
may also be directly produced by salvarsan and in such an event 
the heart shows changes in rate and volume before the blood- 
pressure falls. Sudden death following its administration is there- 
fore generally a cardiac death (Luithlen). 1 The fatal termination 
has also been ascribed (Hoke and Rihl) to a central vasomotor 
depression. The administration of sodium arsenate produces a 
marked fall in blood-pressure without any direct effect upon the 
heart, showing that the action of salvarsan is not identical with 
that of arsenic. In vascular disease, doses which are not toxic to 
the heart may cause a sudden fatal termination through their 
effect on the bloodvessels. Salvarsan causes contraction of the 
coronary arteries and a decreased pulse rate. 2 Rindfleisch has 
emphasized the danger of salvarsan injection in status thymo- 
lymphaticus, and has reported two cases in which a summation of 
depression, salvarsan and thymus extract caused death. 3 

The depression of blood-pressure caused by salvarsan in medicinal 
dosage is never sufficiently great to endanger a normal circulatory 
system, but this form of medication may be definitely dangerous 
in cases of marked hypotension. 4 

Neosalvarsan. — During the administration of neosalvarsan both 
systolic and diastolic pressures, although variable, are usually 
increased apparently as a result of excitement. After the injection 
(seven hours) both pressures are decreased and remain so for several 
days. At first the systolic, later the diastolic, pressure is most 
affected. 3 

Strychnin. — Strychnin is one of the most useful drugs in the 
treatment of symptoms associated with low blood-pressure, 
especially if the vasomotor depression is central in origin. It 
acts reflexly and its beneficial effects are indirect. It is capable 
of increasing the stimulability -of the vasomotor system. 6 Like 

1 Die Exper. Analyse der Salvarsanwirkung, Ztsch. f. exp. Path. u. Therap., 1913, 
xiii, 495. 

2 Cznbalski, F., Abstr. Centralbl. f. d. ges. inn. Med., 1913, iv, 149. 

3 Rindfleisch, W., Status Thymolymphaticus u. Salvarsan, Berlin, klin. "Woch., 
1913, 1, 542. 

4 Sieskind, Das Verhalten des Blutdruckes bei intravenosen Salvarsaninjektionen, 
Munchen. med. Woch., 1911, No. 11. 

5 Rolleston, Influence of Neosalvarsan on Blood-pressure, British Med. Jour., 
1915, ii, 285. 

6 Sollmann and Pilcher, Am. Jour. Phys., 1912, xxx, 369. 



VASOTONIN 343 

caffein, its effects are more pronounced if the blood-pressure is 
subnormal. Marvin 1 found a marked increase in pressure after 
doses of gr. -jV to 2V in healthy students, but practically no results 
from smaller doses. The pulse rate was invariably slowed. The 
recent investigations of Newburgh 2 have shown, however, that in 
infectious diseases in medicinal doses, strychnin does not increase 
the cardiac output, slow the pulse, or materially increase blood- 
pressure. Nor is strychnin of value as a heart stimulant in acute 
or chronic cardiac failure. 3 

Thyroid Extract. — Injected intravenously, thyroid extract pro- 
duces, as do the extracts of most tissues and organs, a fall of blood- 
pressure. It has been suggested that the hypotensive effect of 
thyroid substance is due to cholin, but Vincent believes that the 
depressor effect is due to other substances. 

Since a diminished thyroid secretion or an increased adrenal 
secretion tends to raise blood-pressure, and since these secretions 
appear to neutralize each other, and as exophthalmic goitre patients 
often have relaxed peripheral bloodvessels, the administration of 
thyroid gland seems justified as a therapeutic measure in hyper- 
tension. It stimulates thyroid secretion and cutaneous activity. 
It is best given in small doses, one to three grains daily. Such 
treatment is sometimes attended by beneficial results which not 
infrequently outlast its administration. The experiments of Reid 
Hunt indicate that some of the effects of diet are due to its action 
on the thyroid gland (see Exophthalmic Goitre, page 352) . 4 

Vasotonin ( Yohimbin and Urethane). — The results reported upon 
the use of this drug are contradictory. Favorable action has been 
claimed both experimentally and clinically by some observers. A 
lowering of pressure without depression of the heart or vasomotor 
or respiratory centres has been reported. It is given in 1 c.c. doses 
daily or on alternate days, and may be administered hypodermically . 
It is said to cause less headache than the nitrites, 5 and to produce 
dilatation of the vessels in the extremities especially. It has been 
recommended for angina pectoris and arterial hypertension by 

1 Arch. Int. Med., 1913, xi, 418. 

2 Newburgh, L. H., Strychnin and Caffein as Cardiovascular Stimulants in Acute 
Infectious Disease, Arch. Int. Med., 1915, xv, 458. 

3 Newburgh, L. H., On the Use of Strychnin in Broken Cardiac Compensation, 
Am. Jour. Med. Sci., 1915, cxlix, 696. 

4 Hunt, Jour. Am. Med. Assn., October 19, 1907, p. 1323; September 23, 1911, 
p. 1032. 

6 Mueller and Fellner, Ueber Vasotonin, ein neues druckherabsetzendes Gefaess- 
mittel, Therap. Monatshefte, 1910, xxiv, 285. 



344 EFFECTS OF DRUGS ON BLOOD-PRESSURE 

Fellner 1 who reports favorable subjective and objective results. 
He states that it does not produce the aphrodisiac effects of yohim- 
bin, nor does it produce cardiac depression. 

Veratrum Viride. — Is chiefly employed by some physicians to 
lower blood-pressure in eclampsia. Just why is difficult to under- 
stand, since the drug is not a vasodilator. In small doses it "exer- 
cises its effect upon blood-pressure neither peripherally through 
its action on the vessel walls, or on the vasomotor nerve endings, 
nor through a direct action on the vasomotor centre or on the heart, 
but reflexely through the afferent vagus fibers." 2 Clinically this 
drug has never been widely used because of its danger, uncertainty 
of action, and because its pharmacological status is still unsatis- 
factory. It is usually employed in the form of the tincture in doses 
of 10 to 20 minims. The effective therapeutic dose of the tincture 
of veratrum album, according to Collins, 3 ranges between 30 and 
75 m. Such doses reduce the pulse rate from 12 to 42 beat per 
minute, and lower blood-pressure in both its phases about 30smm. 
Hg. In hypertensive cases the systolic pressure may be even more 
reduced, but the diastolic pressure is much less affected. 

Yohimbin. — Pongs 4 reports in twenty-two cases after doses of 
0.5 to 2 cm. a slight fall of pressure followed by a secondary rise 
up to 35 per cent., reaching its high point in forty-five minutes 
and lasting one to five hours. No hypotensive effects were demon- 
strable even with larger dosage; no untoward results — uremia, 
angina pectoris — were noted. Genital manifestation occurred 
only twice. 

THE EFFECT OF DRUGS ON THE CORONARY ARTERIES. 

It seems evident, a priori, that the local effect of different forms 
of medication upon the pressure and blood-flow in the coronary 
arteries must be of extreme importance in the selection of our 
therapeutic remedies. The circulation in the coronary arteries 
is directly dependent upon blood-pressure. 

This question has been studied experimentally by noting (1) the 
contraction or relaxation of arterial strips, and (2) the amount of 
blood-flow from an opened artery. Such investigations have, 

1 Klinische Erfahrungen iiber Vasotonin, Kong. f. inn. Med., 1910, xxvii, 647. 

2 Cramer, W., The Action of Veratrum Viride, Jour. Pharm. and Exper. Therap., 
1915, vii, 64. 

3 Collins, R. J., The Clinical Actions of Veratrum, Arch. Int. Med., 1915, xvi, 54. 
' Ztschr. f. exp. Path. u. Therap., 1912, x, 479. 



EFFECT OF MEDICATION ON VENOUS BLOOD-PRESSURE 345 

however, not led to uniform results, because, as Rabe 1 discovered, 
in either method the experimental heart is deprived of the effect 
of the central nervous system and is functionating under abnormal 
conditions. 

Voegtlin and Macht 2 found that digitoxin, digitalin, strophan- 
thin, and buffagin produced contraction, and that the nitrites and 
digitonin, digalen, dilatation, of the coronary artery. If these 
findings hold good under normal conditions they would in a measure 
justify the coincident use of the nitrites with digitalis or strophan- 
thus. Rabe noted contraction from strophanthin, digitalein, epi- 
nephrin, and slight contraction from sodium nitrite and caffein. 
Myer's experiments (dogs and cats) corroborate the belief that 
epinephrin dilates the coronary arteries and increases blood-flow 
through them. 3 An increase of the CO2 content of the blood causes 
dilatation of the coronary arteries, together with cardiac dilatation 
and a fall of blood-pressure. Experimental asphyxia causes an 
even greater coronary dilatation, which increases in proportion to 
increased demands upon the heart muscle. 4 



THE EFFECT OF MEDICATION ON VENOUS BLOOD- 
PRESSURE. 

The experiments of Capps and Mathews 5 carried out upon dogs 
under light ether anesthesia yielded the following results: 

The Digitalis Group. — The venous pressure was not materially 
altered. 

Epinephrin. — Small doses produced no effect. Large doses 
caused a rise of from 10 to 80 mm. The rise in venous pressure 
was coincident and coextensive with halting irregular heart action, 
and presumably the result of it rather than dependent upon veno- 
motor stimulation. 

Pitmtrin. — Acted similarly to, but more feebly than epinephrin. 

Caffein. — This drug had no appreciable effect. 

1 Die Reaction der Kranzgefasse auf Arzneimittel, Ztschr. f. exp. Path. u. Ther., 
1912, xi (bibliography). 

2 Jour. Pharm. and Exper. Therap., September, 1913. 

3 Myer, Zur Frage d. Adrenalin Wirkung auf d. Coronarkreislauf, Berlin klin. 
Woch., 1913, 1, No. 20. 

4 Markwalder and Starling, A Note on Some Factors which Determine the Blood- 
flow through the Coronary Circulation, Jour. Physiol., 1913, xlvii, 275. 

5 Venous Blood-pressure as Influenced by the Drugs Employed in Cardiovascular 
Therapy, Jour. Am. Med. Assn., 1913, lxi, 388. 



346 EFFECTS OF DRUGS ON BLOOD-PRESSURE 

Strychnin. — Had no effect on venous pressure except in toxic 
doses, in which it caused a rapid increase of pressure. 

The Nitrites. — Both inhalation and injection of these substances 
caused a decided fall in venous pressure, due apprently to depres- 
sion of the peripheral venous nerve endings. 

Morphin. — This drug in small doses had little effect; in large 
doses it lowered venous pressure, but not nearly to the extent that 
did the nitrites. 

Alcohol. — Large doses increased venous pressure in proportion 
to the degree of cardiac and arterial depression produced. 



CHAPTER XV. 

METABOLIC DISEASES AND MISCELLANEOUS 
CONDITIONS. 

Diabetes. — Experimental Evidence. — Recent researches indicate 
that glycosuria is in some way related to the secretion of the adrenal 
glands. Sugar excretion can be induced by the injection of epi- 
nephrin. The latter also produces a marked rise of blood-pressure 
through vasoconstriction. Neubauer's 1 investigations have shown 
that other substances which raise blood-pressure (e. g., barium 
chloride) may also induce glycosuria, whereas narcotic drugs, 
opium, chloral, alcohol, etc., which tend to lower blood-pressure, 
may diminish or prevent the occurrence of glycosuria after puncture 
of the roof of the fourth ventricle. It has further been shown that 
when sugar excretion is brought about by vasoconstrictor drugs 
it is associated with marked hepatic hyperemia. A local stasis 
of blood in the liver will, it seems, bring about this liberation of 
glycogen in the form of glucose, with an attendant hyperglycemia 
and a glycosuria. It appears that transient glycosuria may be 
brought about by the same emotional states — pain, rage, fear, 
excitement — as those which cause an increased outpouring of epi- 
nephrin into the blood-stream. Until the pathogenesis of diabetes 
has been more thoroughly established no definite conclusions 
regarding the relationship of arterial hypertension to this disease 
can be drawn. The evidence at hand, however, suggests that a 
general vasoconstriction, when accompanied by a local vasodilatation 
of the hepatic vessels, may account for some cases of glycosuria. 
Hagelberg found the sugar content of the blood abnormally high in 
twenty-six cases of nephritis or arteriosclerosis, and suggested that 
an increased adrenalin content of the blood accounts for both the 
hyperglycemia and the hypertension. 2 It is more likely, how- 
ever, that the relationship between hypertension and glycosuria 
is not a causal one. There is no constant relation between blood 

1 Uebcr d. Wirkung antiglycosurischer Mittel u. iiber Leberglucosurie, Biochem. 
Ztsehr., 1912, xliii, 335. 

2 Hagelberg, Berlin klin. Woch., October 7, 1912. 



348 METABOLIC DISEASES 

sugar and blood-pressure, nor is there a sufficient reason for as- 
suming that these two conditions are dependent upon a common 
etiologic factor (epinephrin) . (See Hyperglycemia, page 285.) 

Clinical Consideration. — Diabetes bears no constant relation to 
blood-pressure. Cases occurring in advanced life often show hyper- 
tension as the result of renal and cardiovascular complications, 
which are commonly associated lesions. Jane way found high 
blood-pressure in 50 among 220 diabetics. Diabetes in the young 
is accompanied by normal pressures. In the later stages hypo- 
tension may occur. Blood-pressure estimations may be of diagnostic 
value in differentiating between diabetic and uremic coma. In the 
latter condition hypertension is the rule until the terminal^fairof 
pressure occurs, whereas diabetic coma is associated with hypo- 
tension. 1 Although this occurs less constantly than does hyper- 
tension in uremia, it is sometimes an early manifestation. The so- 
called " diabetic collapse" which has been believed to occur indepen- 
dently of coma, appears to be the result of a rapid fall in blood- 
pressure due to cardiac and vasomotor weakness, resulting from 
acidosis. Experimentally the injection of B-oxybutyric acid causes 
a fall of blood-pressure. 

The pulse rate is increased in diabetes, and, as has been 
emphasized by Benedict and Joslin, stands in intimate relation 
with increased metabolism. 2 Preceding the onset of coma, blood- 
pressure falls sometimes 40 to 50 mm. Hg. Decrease of infra-ocular 
tension, which occurs simultaneously, is well known and results, 
in part at least, from the lowered arterial tension. Blood-pressure 
readings are therefore of value in detecting the onset of coma as 
well as in indicating treatment. It has been found that in coma 
cases with low blood-pressure better results are obtained when 
cardiovascular stimulants are combined with the usual alkaline 
therapy. The administration of thyroid substance to diabetics 
often causes a rise of blood-pressure (Biedl). 

Gout. — Until the pathogenesis of gout is more definitely elu- 
cidated it is impossible to make positive statements in regard to 
the relation of this disease to arterial hypertension. It seems that 
the products of protein metabolism, if increased or abnormal in 
character owing to overeating, suboxidation, or faulty excretion, 
may produce hypertension. Occasionally metabolic intoxication 

1 Ehrmann, R., Ueber cardiovasculare Symptome u. d. Therap. bei diabetischem 
Coma u. Praecoma, Berlin klin. Woch., 1913, 1, 11, 1423. 

2 Metabolism in Severe Diabetes, Carnegie Institute of Washington, 1912, Pub. 
176, 85. 



ADDISON'S DISEASE 349 

seems to lead to hypotension. High pressure is, of course, the rule, 
with added increments of tension during the acute attacks (pain) , 
but gout is very commonly associated with arteriosclerosis and 
chronic nephritis. The latter certainly accounts for a measure, 
if not all, of the increased blood-pressure. Hypotension is some- 
times seen in the later stages in association with cachexia, acidosis, 
and cardiac weakness. It has also been described as occurring 
at the onset of an acute attack. The presence of hypertension 
may be of some value in diagnosticating between lesions of the 
joints, skin, eye, etc., as to whether they be tuberculous or gouty 
in origin. 

Experimental Data. — Investigations point strongly to the conclu- 
sion that the occurrence of gouty symptoms is closely associated 
with abnormalities of protein metabolism, especially with that 
portion of it which relates to the breaking down and elimination 
of the amino-acids. 

In animals the intravenous injection of guanin (0.02 to 0.03 gm. 
per kilo) causes a fall of blood-pressure of from 2.4 to 4 c.c. Hg. If 
other substances are employed which stand chemically near to 
guanin but have no animo group, e. g., xanthin, uric acid, an increase 
of pressure results (0.7 to 2.6 cm. Hg.). In the transition from 
guanin to uric acid there is a splitting off of the animo group, to 
which guanin probably owes its pressor effect. 1 

Jaundice. — Jaundice is often associated with hypotension. 
According to Federn, the latter can often be demonstrated before 
the bile appears in the urine. 

Addison's Disease. — Arterial hypotension is frequently but not 
invariably found in Addison's disease. It bears no relation to the 
degree of pigmentation, but is believed to occur when the medullary 
portion of the adrenal gland is diseased. This tends to corroborate 
the belief generally held at present that the adrenal secretion may 
raise blood-pressure, but that it is not under normal conditions 
the sole cause of its maintenance, 2 and further, that Addison's 
disease results not merely from degeneration of the adrenal glands 
but from involvement of the entire chromaffin system. 

Grunbaum found the oral administration of epinephrin, while 

1 Desgres and Dorleans, Influence de la constitution des corps purques sur leur 
action vis-a-vis de la pression arterielle, Compt. rend. Acad, des Sciences, Paris, 
1913, clvi, 93. 

2 Hoskins, R. G., and Rowley, W. N., The Effects of Epinephrin Infusion on Vaso- 
motor Irritability, Am. Jour. Physiol., 1915, xxxvii, 471; also Cannon, W. B., Bodily 
Changes in Pain, Hunger, Fear, Rage, New York, 1913. 



350 METABOLIC DISEASES 

it did not raise blood-pressure in health, did so in case of adrenal 
insufficiency. He suggests the use of this substance as a diagnostic 
test. Together with careful blood-pressure readings, three grains 
of adrenalin are administered thrice daily. Any distinct subsequent 
rise of pressure in the absence of a valvular lesion is, he believes, 
suggestive of Addison's disease even in the absence of asthenia and 
pigmentation. Too much reliance must not be placed upon this 
test. 

On the other hand, recent experiments have shown that a fall 
of pressure occurs after the injection of dilute solutions of epinephrin, 
and that hypertension occurs only when abnormally large doses 
are used. In amounts sufficient to raise blood-pressure, intestinal 
peristalsis is completely inhibited. If these observations are cor- 
rect the low pressure seen in adrenal insufficiency and in Addison's 
disease are probably due rather to an interference with muscular 
metabolism, including that of the heart and the arteries, than to 
failure of a normal tonic stimulation of the sympathetic nervous 
system. 1 

Auto-intoxication. — Much has been written and but little is 
known regarding gastro-intestinal auto-intoxication. The literature 
on the subject is enormous and concerns itself mainly in nebulous 
hypothecation. It has been shown that two pressor bases may 
be extracted from putrid meat, and the assumption that they 
are generated in the intestine through bacterial action seems 
probable. Granger was unable to confirm the observation of 
Abelous and Bain that the normal urine contains pressor bases, 
and there is as yet no definite clinical proof that these urinary 
pressor substances are identical with those isolated from decaying 
proteids. 2 

Hydroxyphenylethylamin is a substance which can be prepared 
from tyrosin, a derivative of protein cleavage, by splitting off 
carbon dioxid from the tyrosin molecule. This reaction may be 
caused by putrefactive bacteria. Hydroxyphenylethylamin has 
been isolated by Barger 3 from putrefying proteids and shown 
to have a pressor action. The group of aromatic amins to which 

1 Hoskins and McCIure, Am. Jour. Phys., 1912, xxxi, 59; Hoskins and McPeek, 
The Effects of Adrenal Massage in Blood-pressure, Jour. Am. Med. Assn., 1913, 
lx, 1777. 

2 Granger, A. S., Concerning the Presence in the Urine of Certain Pressor Bases, 
Arch. Int. Med., 1912, x, 202. 

3 The Isolation of Pressor Principles of Putrid Meat, Jour. Physiol., 1908, xxxviii, 
341. 



EFFECTS OF GLANDULAR AND TISSUE EXTRACTS 351 

it belongs is related chemically to epinephrin. It is an interesting 
fact that this aromatic amin (p-hydroxyethylamin) with its blood- 
pressure-raising qualities is found in epinephrin, in ergot, and as 
the result of bacterial putrefaction. "Our poisons and our drugs 
are in many instances the close relatives of harmful compounds that 
represent the intermediary steps in the daily routine of metabolism." 
As Abel 1 has recently stated, "It would appear that we have at 
last got onto the right road for the chemical investigation of alimen- 
tary toxemia and its alleged consequences, such as arteriosclerosis 
and chronic renal disease. Phenylalanine, tyrosin, tryptophane and 
histidine, the harmless precursors of toxic amins are always 
present in the intestine, and when they are acted upon by an exces- 
sive number of certain microorganisms the resulting toxic bases 
will surely be formed in excess. If they are then taken up into 
the blood in quantities too large for transformation by the liver 
or other defensive organs, into harmless derivations, they must 
inevitably manifest their pharmacological and toxicological prop- 
erties." 

Not only arterial hypertension but also hypotension has been 
clinically attributed to alimentary toxemia. That the latter no 
less than the former may have basis in fact is shown by the 
observation of Barger and Dale 2 who were able to obtain a highly 
toxic depressor base — B-amino-azolylethylamin from the intestinal 
mucosa. 

This substance appears to be formed from histidine through the 
agency of the B-aminophilus intestinalis. 3 It has further been 
suggested that the toxic substance which causes anaphylactic 
shock bears an allied chemical composition. 

The Effects of Glandular and Tissue Extracts. — The extracts 
of most animal tissues when injected intravenously lower blood- 
pressure. It has been suggested that in many instances this 
depressor action is due to cholin, a substance abundantly found in 
brain-tissue extracts and in tissues in which proteolytic changes, 
which occur very early, have taken place. The action of cholin 
is characterized by the fact that the first injection fails to establish 
tolerance to a second injection, and by the fact that the reaction 
may be counteracted by atropin. The depressor effects of peptone 

1 The Blood and the Specific Secretory Products of the Organs of Internal Secre- 
tion, Science, 1915, N. S., xlii, 165. 

2 Jour. Physiol., 1910, xl, 38. 

3 Berthelot and Bertrand, Compt. rend, de l'Acad. d. Sciences, 1826, cliv, 1643. 



352 METABOLIC DISEASES 

have long been known, but in this case tolerance is established 
by the first dose 1 (see Toxic Shock, page 210). 

Certain glandular extracts have also been shown to possess a 
specific action on blood-pressure. Thus extract of the adrenals 
and hypophysis possess well-marked pressor effects, while pineal 
and thyroid extracts cause a fall of pressure. 

Acromegaly. — In acromegaly pressure is variable (see Pituitary 
Extract, page 340). Chronic hypopituitarism, both clinical and 
experimental, is characterized by a deposition of fat, a lowering of 
body temperature, a retardation of the pulse and respiratory 
rates, somnolence and lowered blood-pressure. These symptoms, 
as has been pointed out by Cushing and Goetch, 2 bear a striking 
resemblance to the state of hibernation as it occurs in some animals. 
W. Landon Brown 3 states that in the early stages of acromegaly 
in association with hemianopia, lowered sugar tolerance and osseous 
hypertrophy, blood-pressure is high, whereas in the later stages 
with a high sugar tolerance blood-pressure is low. In Frolich's 
syndrome (primary hypopituitarism) smooth, dry skin, scant pubic 
and axillary hair, small, thin finger-nails — blood-pressure is low. 

Exophthalmic Goitre. — Experimental Data.— In 1894 Oliver and 
Schafer reported that the intravenous injection of aqueous or 
glycerinized extracts of the thyroid gland produced a fall of blood- 
pressure in which the heart took no part. These observations 
have been widely corroborated. A few observers found an increased 
pressure and local vascular constriction after thyroid injections. 
The pulse rate has been reported both as accelerated and retarded. 

Von Cyon and Oswald found lowering of pressure and slowing 
of the pulse after the intravenous injection of iodothyroid even 
after atropinization and section of the vagi. Later experiments 
have shown that the effect of this substance upon cardiac inhibition 
is questionable, and that the fall of pressure is not a specific action, 
but occurs after the injection of many organic extracts which 
contain cholin, a substance which is associated with the metabolism 
of lethicin and other lipoids, and to which the fall of blood-pressure 
is due. On the other hand, it has been maintained that the fall of 
pressure is not due to a cholin but to. a specific substance, vaso- 
dilatonin (Popielski), which acts even after atropinization. This 

1 Sanford and Blackford, Comparative Study of the Effects on Blood-pressure 
of the Extracts and Serums of Exophthalmic Goitre and other Substances, Jour. 
Am. Med. Assn., 1914, lxii, 117 (bibliography). 

2 Jour. exp. Med., 1915, xxii. No. 1. 

3 Physiological Principles in Treatment, London, 1914, p. 34. 



EXOPHTHALMIC GOITRE 353 

substance seems not to be a specific thyroid product. In contra- 
distinction to the equivocal results in dogs and rabbits, in cats 
iodothyroid produces a marked lowering of blood-pressure which 
is due to both vascular and cardiac action; but here again it seems 
that similar effects may be produced by other iodized albumins. 
Therefore the contention of von Cyon that iodothyroid possesses 
a fundamental cardiovascular regulatory function has not been 
substantiated, nor has the hypothesis that the cerebral circulation 
is controlled by an interaction between the thyroid, hypophysis, 
and pineal glands any better foundation. The intravenous injection 
of thyroid extract in cats and rabbits increases the stimulability 
of the depressor function and the rise of pressure produced by 
adrenalin (Biedl). 1 

The oral administration of thyroid substance in man produces 
an increased pulse rate and often a fall of blood-pressure; in diabetics 
a rise of pressure occurs which outlasts the employment of the 
medication by several days. The prolonged use of thyroid usually 
produces similar effects, although both experimentally and thera- 
peutically the results are inconstant and have again been explained 
as not due to specific thyroidal action (Biedl). Blackford and 
Sanford found that a powerful depressor substance exists in 
exophthalmic goitre cases and that a primary injection establishes 
tolerance to the action of any further administration. Atropin 
does not inhibit its action, but heating to 70° C. does, hence the 
substance does not behave physiologically like cholin. The action 
is chiefly the result of peripheral vasodilatation associated with 
some diminution of the systolic output. Irritability of the vagus 
is not decreased. The existence of a crossed tolerance between 
the depressor action of extract of exophthalmic goitre and of serum 
from patients suffering from this disease suggests that the two 
substances are identical. 2 

Clinical Data. — Clinical reports of blood-pressure findings in 
exophthalmic goitre are divergent. Some observers report hyper- 
tension and some hypotension, as a characteristic finding. Arterial 
tension is often -variable and labile. The very high readings of 
some cases are not part and parcel of the disease, but result from 
arteriosclerotic changes which occur early in these cases as the 
result of prolonged wear and tear (Muenzer). The question as to 
whether exophthalmic goitre results from a mere quantitative 

1 Innere Sekretion, 1913, i, 205. 

2 Blackford, J. M., and Sanford, M. D., Med. Record, 1913, lxxxiv, 379. 
23 



354 METABOLIC DISEASES 

increase or from a qualitatively abnormal thyroid secretion is 
still unsettled. Plummer 1 has put forth the suggestion that the 
(systolic) hypertension which he usually found in exophthalmic 
goitre, when long continued, not infrequently leads to chronic 
arterial hypertension. 

As might be expected from the symptoms of this disease, flushing, 
warmth, perspiration, and a rapid pulse, blood-flow is rapid. 
Stewart found in a case studied by him that immersion of one 
hand in cold water reduced the flow in its fellow from 14 to 7 gm. 
per 100 c.c. per minute. Weber found that in exophthalmic goitre 
and in neurasthenia there was a tendency for the normal vasomotor 
reflexes associated with attention and the suggestion of movement 
to be readily lessened or even reversed: In other words, fatigue 
phenomena occurred more readily than in normal cases. 

McCrea has called attention to a special type of exophthalmic 
goitre associated with a gain in weight, an increased blood-pressure 
(200), a high lymphocytosis and drowsiness. Improvement occurs 
under the use of thymus extract. 

Kaess 2 found the viscosity of the blood in exophthalmic goitre 
normal in 19 per cent., decreased in 50 per cent., and increased in 
31 per cent, of his cases. The latter occurred in the vagotonic cases 
and probably resulted from increased perspiration, diarrhea, etc. 
Diminished viscosity occurred in the sympathicotonic cases and 
was perhaps due to abnormality of the serum. Hemic viscosity, 
however, bears no constant relation to blood-pressure. There is 
no constant relation between the severity of the disease and vas- 
cular tension, although, as a general rule, the worst cases show a 
low pressure. 3 Pressure changes are probably due to both the 
heart and the vasomotor system. 

Periarteritis Nodosa. — Although Meyer, in 1878, believed that 
this disease was due to high blood-pressure which caused a rupture 
of the arterial media, recent investigations point to an infectious 
origin. In 5 of the 38 cases of this disease collected by Lamb 4 the 
blood-pressure readings were reported as 140, 215, 77-100, 130-165, 
104, showing therefore no constant relationship. 

Myxedema. — In myxedema blood-pressure is generally increased. 

Adiposity. — Adiposity is not associated with any constant 
blood-pressure abnormalities. When the circulatory system is 

1 Trans. Assn. Am. Phys., 1915. 

2 Bruns, Beitr. z. klin. Chir., 1912, lxxxii, 253. 

3 Spiethoff, D., Centralbl. f. inn. Med., August 23, 1902. 

4 Periarteritis Nodosa, Arch. Int. Med., 1914, xiv, 481. 






ANEMIA 355 

normal a loss of weight entails no fall of pressure, but if hyper- 
tension is associated with adiposity a reduction of weight produces 
a fall of pressure, 1 largely, it would seem, owing to a diminution 
of metabolic waste products which result from overeating. (See 
p. 2G9). 

Scurvy. — The Capillary Resistance Test. — In the early stages of 
scorbutus, even before other clinical manifestations have occurred, 
a cuff applied to the arm and kept inflated for three minutes will 
cause the appearance of petechial spots. 2 The test is of course 
not specific for scurvy but merely indicates the resistance of the 
capillaries to pressure. 

Status Lymphaticus. — In status lymphaticus we have to do with 
an individual who is constitutionally subnormal. The muscular 
physique is poor and the physical strength and constitutional 
resistance below the normal standard. The blood-pressure is apt 
to be somewhat lower than the subject's age and weight would 
lead us to expect. According to Muenzer, hypotension is found 
associated with lymphocytosis. While this may hold good for 
extreme cases, certainly lymphocytosis has not been shown to be 
a constant phenomenon in adults, nor, so far as we are aware, in 
children. Operative procedures in this class of cases are dangerous, 
especially if chloroform is used as an anesthetic. The toxemia of 
acute infectious disease is also badly borne by these patients. 
Sudden and unexpected death during anesthesia, infections, while 
swimming, or in children while quietly resting in bed, appears to 
bear a relation to enlargement of the thymus gland. The experi- 
mental intravenous injection of thymus substance lowers blood- 
pressure, but whether this results from vasomotor depression or 
from purely mechanical causes (embolism, thrombosis), as suggested 
by Popper, 3 is uncertain. It may also be simply the non-specific- 
fall of pressure which attends the intravenous introduction of 
different foreign proteids. 

Anemia. — Experimental Data. — Loss of blood tends to cause a 
fall of blood-pressure. When hemorrhage has been moderate this 
tendency is compensated by reflex vasomotor constriction and an 
increased pulse rate; when excessive, death occurs with a progres- 
sive fall of pressure, owing to cerebral anemia. 

1 Dunin, Th., Der Blutdruck in Verlaufe d. Arteriosclerose, Ztsch. f. klin. Med., 

1904, liv. 

2 Hess and Fish, Infantile Scurvy, Am. Jour. Child. Dis., 1914, viii, No. 6. 

3 Ueber d. Wirkung d. Thymus extrakts, Sitzungsber. d. k. Akad. d. Wissensch., 

1905, cxiv. 



356 METABOLIC DISEASES 

The quality of the blood exerts an influence on vascular tonus 
and blood-pressure. Lesser found that section of the cord between 
the second and fourth cervical vertebrae caused a fall of pressure 
and a diminution of hemoglobin in the large vessels, whereas 
stimulation of the sectioned cord increased the hemoglobin. Section 
above the splanchnic centre diminishes the erythrocytes (Cohnheim 
and Zuntz). Experimental epinephrin hypertension (in dogs) 
increases the red cells in the capillaries and veins but not in the 
large arteries. According to Erb, the arterial and venous hemic 
concentration increases with a rise and decreases with a fall of 
pressure. Holobuts attributes the variations of the number of 
erythrocytes to changes in the volume . of the corpuscles. The 
dried residue and the plasma show but little change with pressure 
variations (Horner). 1 

Clinical Data. — Blood-pressure observations in the different forms 
of anemia are of little value, except in the detection of nephritic 
complications. If the anemia is marked, pressure will be low in 
proportion to the cachexia and general weakness. Chlorosis is 
said to be accompanied by slight hypertension in the early stages, 
followed later, if its course be prolonged or severe, by hypotension. 
Blood-pressure bears no constant relation to either the percentage 
of hemoglobin or to the total number of corpuscles. According to 
Plesch the minute volume of the heart is increased in the anemias. 
Stewart found peripheral blood-flow in anemia less than normal. 
This peripheral constriction has been construed as a necessary 
compensatory arrangement for increasing blood-flow through the 
lungs. The deficiency in the hand flow is less in chlorotic anemia 
than in the other forms. Muenzer 2 found lymphocytosis frequently 
associated with arterial hypotension. In pernicious anemia very 
low readings are often observed. Cabot states that systolic pressures 
of 80 and even GO mm. are not unusual. 

Cachexia. — Nutritional failure from whatever cause is often 
associated with low arterial pressure, but this is by no means 
invariably the case. The high pressures of nephritis may be some- 
what reduced by the coincident presence of cachexia. A remarkable 
case of persistent hypotension has been reported by Rolleston: 3 
that of a man with carcinoma of the tongue and amyloid disease 

1 Der Blutdruck d. Menschen, Vienna, 1913, p. 101. 

2 Blutdruck u. Blutbild, Med. Klinik, 1913, ix, 2028, 2074. 

3 Low Blood-pressure in Carcinoma of the Tongue with Amyloid Disease. Lancet, 
September 12, 1914, p. 692. 



EFFECTS OF HIGH ALTITUDES ON BLOOD-PRESSURE 357 

who managed to live for several weeks with systolic and diastolic 
pressures of 70 and 35 respectively. 

The Effects of High Altitudes on Blood-pressure. — The disturb- 
ances of physiologic function which result from high altitudes are 
mainly due to a deficiency of oxygen. The vertigo, confusion of 
the senses, and fatigue can be abated by the inhalation of oxygen. 
At altitudes of from 4000 to 8000 meters (13,000-26,000 feet) 
no special precautions are necessary, provided the partial pressure 
of the oxygen in the lungs is raised. Beyond this, special devices 
insuring adequate oxygenation must be employed. Mountain 
sickness results from a combination of diminished oxygen supply 
associated with muscular exertion, producing syncope, a weak 
pulse, and other symptoms of cerebral anemia. Circulatory symp- 
toms are especially apt to occur in aviators if very rapid ascents or 
descents are made. 

Henderson's studies made on Pike's Peak (14,000 feet) showed 
that there was a slight fall of arterial pressure. It seems to be 
generally agreed that altitude of a considerable degree does tend 
to lower blood -pressure and to increase the pulse rate, and that 
these changes are more marked at first, i. e., before "acclimatiza- 
tion" has taken place. Such a fall of pressure may range between 
1 and 22 mm., and the effects are naturally more marked in 
hypotensive individuals. There is, however, a great difference in 
individual susceptibility. The systolic pressure is chiefly and more 
constantly affected, and diastolic pressure may even rise. Ordinarily 
slight elevations produce but little change in blood-pressure. It 
is quite impossible either from a man's general physique or from 
any other criterion to forecast how much his pressure may be 
affected. 1 The rate of blood-flow was increased from 30 to 76 per 
cent., by residence at Pike's Peak. This was associated in part with 
an increased pulse rate and a fall of venous pressure. The arterial 
pressure was not clearly altered either by altitude or by oxygen 
inhalations. The latter did slow the pulse rate 14 per cent, at 
14,109 feet, and 54 per cent, at 6000 feet. 2 The readings obtained 
by Clough at an elevation of over 5000 feet were practically iden- 
tical with those taken at the sea level. Miners in suddenly 
descending or ascending 1700 feet to and from their work show 

1 Schneider and Hedblom, Blood-pressure, with Special Reference to High Alti- 
tudes, Amer. Jour. Physiol., 1908, xxiii, 90. 

2 Schneider, E. E., and Sisco, D. L., Circulation of the Blood at High Altitudes, 
Am. Jour. Physiol., 1914, xxxiv, 1 (literature). 



358 METABOLIC DISEASES 

variations hardly exceeding 5 mm. Hg. 1 Hess 2 has attempted to 
explain the changes in blood-pressure at high altitudes by the fact 
that the normal balance between the concentration of the arterial 
and the venous blood (which he believes is normally regulated by 
the lungs) is upset. 

Doubtless many of the contradictory statements regarding the 
effects of altitude on blood-pressure are due to the fact that normal 
and abnormal subjects have been classed together. Thus among 
tuberculous patients an elevation of 6000 feet appears to increase 
blood-pressure, which on the whole should have a distinctly 
beneficial effect. 3 The rate of blood-flow and of the pulse is markedly 
increased at high altitudes (14,000 feet).. This is associated with 
a fall of venous pressure and with arteriolar dilatation. These 
changes are apparently due to a deficiency of oxygen, since inhala- 
tion of this substance affects both pulse rate and rate of flow. 4 
Altitude has a more pronounced effect upon hypertension due to 
general arteriosclerosis than upon that associated with well-marked 
nephritic lesions 5 (see page 50). 

The question as to the effect of altitude upon the individual is 
an important and practical one. The physician is constantly con- 
sulted regarding the effects of high altitude in tuberculosis, heart 
disease, emphysema, etc. It is generally agreed that residence 
at a high elevation increases the number of erythrocytes and the 
percentage of hemoglobin. There is also reason to believe that 
the cells of the pulmonary alveoli possess and may take on an 
increased capacity to secrete oxygen into the blood. These changes 
are of a compensatory nature. Although the whole question of 
the physiologic effect of altitude is still unsettled, it seems evident 
that the symptoms from which balloonists, aviators, and mountain 
climbers suffer cannot be explained on a basis of blood-pressure 
alterations. 

Plungian's investigations indicate that barometric changes at 
a given altitude exercise an effect upon individual blood-pressure, 

1 Clough, F. E., Blood-pressure Variations as Influenced by Rapid Changes in 
Altitude, Arch. Int. Med., 1913, xi, 590. 

2 Die Beeinflussung d. Fliissigkeits anstauches zw. Blut. u. Geweben durch 
Schwankungen d. Blutdrucks, Deutsch. Arch. f. klin. Med., 1904, lxxix, 128. 

3 Peters and Bullock, Blood-pressure Studies in Tuberculosis at a High Altitude, 
Arch. Int. Med., 1913, xii, 458. 

4 Schneider and Sisco, The Circulation of Blood in Man at High Altitudes, Am. 
Jour. Physiol., April, 1914, xxxiv. 

6 Schrumpf, P., Blutdruckuntersuchungen u. Energometerstudien im Hochge- 
birge bei Herz- u. Kreislaufstorungen, Deut. Arch. f. Klin. Med., 1914, xciii, 4CG. 



LIFE INSURANCE 350 

although this is inconstant, both quantitatively and qualitatively. 
The most marked changes generally occur in tuberculous and 
arteriosclerotic subjects after a sudden fall of the barometer. 1 

The Effects of Tropical Climate. — Much has been written on 
the effects of tropical sunlight on white men. To whatever 
the deleterious effects are due, they are apparently not the result 
of blood-pressure changes. The average blood-pressure of Americans 
in the Philippines is quite similar to that when at home. The lowest 
readings are obtained during the first three months of tropical 
residence and during the hottest months, but the fall of pressure 
is quite inconsequential (3 mm.). No difference has been noted 
among individuals with light or dark complexions, nor when 
different types of underwear are worn. 2 According to McCay 
the pressure of the natives of India is lower than that which obtains 
in western Europe, and yet arteriosclerosis is very common among 
them. Possibly the low protein diet and more constant perspiration 
may have a bearing upon the low pressure. Oliver's investigation 
showed that during prolonged hot weather blood-pressure was 
lowered in the brachial artery, but was increased in the phalangeal 
vessels. 3 

Life Insurance. — The importance of blood-pressure examinations 
as a means of sifting out undesirable "risks" has now become 
generally recognized by life insurance companies and is routinely 
required by many of them. Statistical studies have shown that 
blood-pressure values, abnormal in relation to the age and sex 
of the individual, are definitely associated with a shortened expect- 
ancy of life. It would seem that pressures of 20 mm. either below 
or above the normal standard require an explanation. As has 
been stated elsewhere, high pressures often indicate renal, and 
low pressures, tuberculous disease. 

Fisher 4 has pointed out that a pressure of 150 gives a higher 
mortality than an average risk, and an increase of 15 per cent, 
above the normal pressure for a given age should always excite 
suspicion. Among 2,661 risks with an average pressure of 142.43, 
at the ages of forty to sixty, the mortality was about the same as 

1 Plungian, M., Ueber d. Wirkung athmosphaerischer Einflusse auf d. Blutdruck, 
Dissert. Basel, 1913, p. 43. 

2 Chamberlain, W. P., A Study of the Systolic Blood-pressure and the Pulse, 
Rate of Healthy Adult Males in the Philippines, Philippine Jour. Sci., 1912, vi, 467. 

3 Quoted, Allbutt, Diseases of the Arteries, Including Angina Pectoris, London, 
1915, i, 181. 

4 The Diagnostic Value of the Sphygmomanometer in Examinations for Life 
Insurance, Jour. Am. Med. Assn., 1914, lxiii, 1753. 



360 METABOLIC DISEASES 

the average general mortality of the company, but with an average 
pressure of 152.58 among 525 risks the mortality increased 30 per 
cent, in excess of the average. Among the rejected risks with an 
average pressure of 161 .44 (1970 applicants) the mortality was 190 
per cent, of the medico-actuarial table and more than double the 
average mortality of the company. During the interval of from 
1907 to August 1, 1913, 1970 applicants were refused insurance 
solely on the basis of a pressure of 160 mm. Hg. These cases but 
for the pressure readings would have been accepted. The con- 
tinued accumulation of life insurance statistics will throw much 
light not only upon the diastolic pressure and upon hypotension, 
but also on a large and important class of individuals who have only 
slightly increased pressure, who consider themselves in perfect 
health and do not, therefore, come under the observation of the 
physician. 

As a ready means of calculating what a given individual's blood- 
pressure should be, Faught has suggested the following rule: Assume 
that the normal systolic pressure of a person aged twenty years 
is 120 mm., and add 1 mm. Hg. for each additional two vears 
of life. 

The different phases of blood-pressure as applying generally to 
insurance have been discussed in different chapters of this book. 
The reader is specially referred to Instrumental Technique, page 
125; Sources of Error, page 122; Physiologic Variations with 
Special Reference to Age, page 53; Hypertension in Nephritis, 
page 267; Tuberculous Hypotension, page 213. 

Infants and Children. — Blood-pressure estimations in infancy 
and early childhood are made with difficulty and fraught with 
inaccuracy. The psychic effects produced by the procedure, which 
often result in crying or struggling, absolutely vitiate the accuracy 
of the readings. The arm is too small to permit satisfactory applica- 
tion of the cuff, hence the readings should be taken on the thigh and 
a small cuff (6.5 cm.) employed. As a temporary makeshift the 
usual 12 cm. cuff may be folded in half. The child will pay less 
attention to the cuff when it is applied to the lower extremity. 
The diaper must be loosened. Auscultation is more satisfactory 
than palpation. The diastolic pressure which is determinable 
with difficulty owing to the small size of the artery and of the 
pulse pressure, must generally be estimated either by auscultation 
or by means of a Fedde oscillometer or some similar device. In 
childhood and youth the transmission of the pressure wave from 



INFANTS AND CHILDREN 361 

the centre to the periphery behaves differently than in the adult. 
In the former the systolic pressure in the digital artery equals 
that registered in the brachial, whereas in the adult, especially 
in cases of nephritis and arteriosclerosis, the arterioles are tonically 
contracted as well as less elastic, and the systolic brachial pressure 
is much higher than that in the digital arteries. 1 

The diastolic pressure is relatively higher than in adults. 2 On 
the whole, blood-pressure estimations are of much less value in 
children than in adults. 

Normal Pressure. — Before birth blood-pressure is higher in the 
pulmonic than in the systemic circulation. The expansion of the 
lungs promptly lowers pulmonary blood-pressure. Before this 
occurrence most of the blood passes from the pulmonary artery 
through the ductus arteriosus into the aorta, but afterward, the 
lowering of blood-pressure which occurs in the systemic circulation 
when the placental circulation is cut off, causes a collapse of the 
ductus and thus favors its closure. Additional causative factors 
may be the equalization of pulmonary and aortic pressures and the 
muscularity of the ductus. (Abbott. 3 ) At birth systolic blood- 
pressure is said to range between 35 and 55 mm. Waking and 
suckling cause a rise of about 15 mm. 4 

Preceding the onset of puberty there is a tendency toward a 
fall of pressure, during pubescence there is a period of increased 
pressure which is in turn followed by a slight decrease after puberty 
has been established (Albutt). (See Gonads.) The attempts which 
have generally been made to establish normal standards in relation 
to age have led to more or less confusion. Pressure increases with 
age, and during the first month of life the normal range lies between 
60 and 68 mm. Hg. Some recent investigations have shown that 
blood-pressure increases with height and weight, and that these 
criteria are more definitely fixed than the mere age factor. 5 Further, 
the variations which have been attributed to the influence of sex 
are really dependent upon the effect of height and weight. 

1 Findlay, L., The Systolic Pressure at Different Points of the Circulation in the 
Child and the Adult, Quar. Jour. Med., 1910-11, iv, 489. 

2 Melvin and Murray, Blood-pressure Estimation in Children, British Med. Jour., 
April 17, 1915, p. 2833. 

3 Congenital Cardiac Disease, Osier and McCrae's Modern Med., 1915, iv, 411. 

4 Balard, P., Le Pouls et la Tension Arterielle de l'Enfant et du Nouveau-ne, 
Gaz. des Hop., 1913, lxxxvi, 837. 

Nos. 4-6. 

6 Wolfensohn-Kriss, Ueber Blutdruck im Kindesalter, Arch. f. Kinderheilk., liii, 
Nos. 4-6. 



362 METABOLIC DISEASES 

Table I. — Comparison or Height and Systolic Blood-pressure. 1 

Systolic 
blood-pressure. 
Height. Mm. 

3 feet 6 inches 99 

4 feet to 4 feet 3 inches 109 

4 feet 3 inches to 4 feet 6 inches 112 

4 feet 6 inches to 4 feet 9 inches 118 

4 feet 9 inches to 5 feet 120 

5 feet 125 

Table II. — Comparison of Weight and Blood-pressure. 

Elood-pressure. 

Weight. Mm. 

30 to 40 lbs 95 

40 to 50 " 100 

50 to 60 " " 107 

60 to 70 " 112 

70 to 80 " . . 116 

80 to 90 " 122 

90 to 100 " 126 

The foregoing facts explain the statement frequently made 
that "robust" children have higher pressures than delicate ones, 
and perhaps also that breast-fed infants give higher readings than 
those artificially nourished. Popoff 2 found the systolic and dias- 
tolic pressures in the newborn infant to average 75 and 34 mm. 
Hg. respectively. Prematurely born infants had lower pressures 
(see page 53). Laitao found that at the end of seven months the 
systolic pressure was generally 100 mm., and that the pulse press- 
ure which during the first month averaged 18 mm., at the end of 
the first year had reached 28 mm . 3 These values are higher than 
those obtained by Kaupe, 4 who found an average pulse pressure 
of 8 to 10 mm. Hg. , 

In infants after feeding the pressure is increased 8 to 10 mm., 
and during sleep pressure ranges between 60 and 70 mm. In 
children an hour's exercise may elevate the pressure 5 to 10 mm., 
at which point it may remain for half an hour (Trumpp) (see also 
Acute Infections, page 196). 

Blood-pressure and Physical Efficiency. — Studied from the 
standpoint of the "Intercollegiate Standard," which consists of 
adding the strength of the back, plus that of the legs, plus that of 
the right and left forearms, plus the lung capacity divided by 20, 
plus bodily weight divided by 10 and multiplying the last figure by 

1 Michael, M., A Study of Blood-pressure in Normal Children, Amer. Jour. Dis. 
Children, 1911, i, 272. 

2 Beitrage z. Frage nach d. Blutdruck b. gesunden Kindern, Dissert. St. Peters- 
burg, 1913, p. 200. 

3 Laitao, M., Pression Arterielle chez l'enfant, Arch. d. Mai. d. Enfants, 1913, 
xvi, 102. 

4 Der Blutdruck im Kindesalter, Monatsschr. f. Kinderheilk., 1910, ix, 257. 



BLOOD-PRESSURE AND PHYSICAL EFFICIENCY 363 



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364 METABOLIC DISEASES 

number of times the subject is able to dip his body by the strength 
of his arms and shoulders, Baraeh and Marks found that there is 
no constant relation between physical efficiency (which also means 
circulatory efficiency), and either the pulse pressure, diastolic 
pressure ratio, nor between the pulse-pressure percentage of the 
diastolic pressure. 

The following tables compiled by Baraeh and Marks 1 show the 
actual systolic and diastolic pressures encountered among 742 
male students: 

Table I. — Age Distributing in a Series of 552 Consecutive Cases. 

Age, yeais. Cases. 

15 to 17 27 

17 to 19 200 

19 to 21 202 

21 to 23 71 

23 to 25 31 

25 to 27 12 

27 to 29 6 

29 to 31 1 

Over 31 2 

Total 552 

Table II. — Distribution of Maximum Pressure in 656 Cases. 

Mm. Hg. Cases. 

90 to 100 7 

100 to 110 23 

110 to 120 112 

120 to 130 204 

130 to 140 153 

140 to 150 95 

150 to 160 45 

160 to 170 14 

170 to 180 1 

180 to 190 \ 3 

190 to 200 J 

Total 656 

Table III. — Minimum Pressure Read at the Last Clear Sound 

Mm. Hg. Cases. 

40 to 50 1 1 

50 to 60 4 

60 to 70 12 

70 to 80 41 

80 to 90 94 

90 to 100 121 

100 to 110 27 

110 to 120 9 

120 to 130 3 

Total 312 

1 Blood-pressure, their Relation to Each Other and to Physical Efficiency, Arch. 
Int. Med., 1914, xiii, 64S. 



273 cases or 87 % 



EFFECT OF MARATHON RACES 305 

The foregoing tables are taken from Judson and Nicholson, 1 
who include their own figures based upon a study of 2300 children. 
As these authors point out, "The widest variations occur from the 
tenth to the fourteenth year when there is a marked rise in the 
systolic pressure. From the fourth to the fourteenth year, inclusive, 
the variations do not exceed 5 mm. in two-thirds of the cases." 
Their systolic readings were higher than those previously obtained 
by others. There is a gradual rise of pressure as age increases 
between the ages studied, amounting in all to 14 mm. Hg. Up to 
eight years of age a 9 cm. cuff gives accurate readings, but after 
eight years a 13 cm. armlet should be employed. The onset of the 
fourth auscultatory phase (muffling) must be used as the criterion. 

Athletics. — The physician is frequentl}' consulted regarding the 
advisability of allowing certain individuals with functional or 
organic heart lesions to indulge in athletic exercises. The -tendency 
at present is certainly to be more liberal in what may be allowed 
that was formerly the case. This is specially true of children 
and young adults with heart murmurs. Before assenting to or 
advising such procedures, however, we must realize that although 
exercise is as necessary for the heart as for any other muscle, yet 
certain forms of exercise throw an enormous burden upon the cir- 
culatory apparatus (see pages 46 and 300). 

The more sudden and violent the exercise (sprinting, hammer 
throwing, etc.) the greater the rise of blood-pressure (200 mm.) 
and the more rapid the pulse. Endurance exercises (long distance 
running, etc.) produce a more gradual and less extreme rise of 
pressure, but a pressure which remains high for a longer time. The 
sudden changes of pressure in the former group probably do no 
harm to young normal individuals with resilient arteries, but they 
should be avoided by elderly men in whom permanent cardiac 
dilatation may result. The prolonged strain of endurance exercises 
among young growing children should certainly not be encouraged 
(McKenzie) . 

The Effect of Marathon Races. — Before the Race.— Most of the 
men had trained for six to nine months preceding the race of twenty- 
four miles. Most of the men showed evidences of cardiac enlarge- 
ment and had a slower pulse rate than normal. The cases which 
showed a more than average diurnal pulse variation also showed a 
cardiac hypertrophy and an increased blood-pressure. The highest 

1 Blood-pressure in Normal Children, Am. Jour. Dis. Children, 1914, xii, 257. 



3GG METABOLIC DISEASES 

blood-pressures were found in coincidence with the largest hearts. 
The men who had heart murmurs had even larger hearts and higher 
pressures. As one would expect the men who were overweight, 
whose occupations were laborious, and whose periods of preliminary 
training were short, showed higher than average cardiac enlargement 
and blood-pressures. 

After the Race. — The average fall of blood-pressure was 20 mm. 
Cases with heart murmurs showed an even greater drop. Some 
cases showed marked cardiac dilatation (x-ray), and in these 
blood-pressure was lower than in those whose heart dilated less. 
At the end of six months both heart and blood-pressure examina- 
tions yielded normal findings in most of the cases but some 
increased much more slowly than others. i 

If there is any doubt whatever regarding the organic character 
of a murmur it is better to err on the safe side and advise against 
prolonged or severe forms of athletics. 

Much has been written of late concerning the evil effects of over- 
athleticism, and regarding this subject there is much difference of 
opinion. 

Severe exercise of an hour has been shown to not infrequently 
cause the appearance of albumin, casts and blood cells in the urine 
of healthy subjects, phenomena which are doubtless clue to circula- 
tory changes in the kidney at a time when waste products in large 
amount must be eliminated. 2 

Prolonged and severe athletic training produces demonstrable 
cardiac hypertrophy with increased blood-pressure. These phe- 
nomena may be transient and ephemeral, but they are not 
always so. 

It certainly does not seem reasonable to believe that Marathon 
races run by poorly developed and untrained individuals as we often 
see them in our city streets, can be beneficial. Xor does it seem 
logical to assume that four-mile boat races at the end of which even 
trained athletes go into a state of syncope, can be considered 
healthful exercise. It is believed by some that strenuous athletics 
use up an individual's reserve force — his vital reserve. Whether 
this be so or not cannot be proved, but certainly the picture of the 
husky giant who succumbs in the early stages of typhoid fever or 
pneumonia is an all too common one. 

1 Savage, W. L., Physiological and Pathological Effects of Severe Exertion (The 
Marathon Race), Am. Phys. Educ. Rev., 1910, xv, No. 9; 1911, xvi, Nos. 1-5. 

2 Barach, J. H., Against Overathleticism, Trans. IV International Congress of 
School Hygiene, Buffalo, August, 1913. 



BLOOD-PRESSURE IN CASTRO-ENTERITIS 367 

It is very questionable whether in the ordinary course of life, 
the "athletic heart" is an asset. Investigations among the athletes 
at the University of Wisconsin have shown cardiac abnormalities 
among a considerable proportion of the athletes. 1 This has been 
attributed by some apologists to faulty methods of training. The 
report of the Surgeon-General of the United States Navy attributes 
a large excess of deaths attributable to cardiac overstrain among 
the cadets at Annapolis, to overathleticism. In cardiac cases the 
physician carefully questions the patient regarding antecedent 
infections, but rarely in regard to athletic overindulgence or 
mishaps. 

It seems merely conservative, therefore, to insist that competitive 
athletics should be conducted only under competent medical 
supervision, and that growing boys should not be allowed to indulge 
in the prolonged and exhausting competitions, which greatly tax 
even a fully developed heart. 

The Effect of Athletic Training. — Training renders an individual 
more efficient (1) by increasing cardiac and vasomotor responses 
to meet sudden or prolonged demands for physiological activity; 
(2) by educating the brain centres so that muscular actions become 
semi-automatic and hence less volition is required in their perform- 
ance; (3) by accustoming the medullary centres to an increased 
quantity of carbon dioxid; and (4) by increasing the rate of ex- 
cretion of waste products of metabolic activity. 

Middleton 2 has found that training during a football season 
produces fairly uniform results which may be expressed as follows: 

1 . A proportionate decrease in both systolic and diastolic pressure 
during the training period. 

2. After the rest following the training season a rise of both 
pressures occurs which exceeds the ante-season records. 

3. The blood-pressure reaction to a test of fifty stationary 
running steps is practically unaltered by the training. 

The decrease in the blood-pressure mentioned may be due to 
peripheral vascular relaxation or to cardiac dilatation, or to a 
combination of both factors. 

Blood-pressure in Gastro-enteritis. — The suggestion has been 
made that the collapse which occurs in the course of epidemic 
diarrheas is in part due to a fall of blood-pressure resulting from 

1 Schumacher, L., and Middleton, W. S., The Cardiac Effects of Immoderate 
College Athletics, Jour. Am. Med. Assn., 1914, lxii, 1136. 

2 The Influence of Athletic Training on Blood-pressure, Am. Jour. Med. Sci., 
1915, cl, 426. 



368 METABOLIC DISEASES 

loss of fluid in the tissues and producing anuria, and that saline 
infusion should be used in combating this symptom 1 (see Cholera, 
page 199). 

Vomiting causes a fall of blood-pressure which is in part due to 
the cardiac inhibition which occurs when the vomiting centre is 
stimulated 2 not only a fall, however, but very sudden and extensive 
pressure variations are also met with. 3 

i British Jour. Child. Dis., 1912, ix, 343. 

2 Miller, Am. Jour. Physiol., May, 1915. 

3 Brooks and Luckhardt, Blood-pressure during Vomiting, Am. Jour. Physiol., 
1915, xxxvi, 104. 



CHAPTER XVI. 
DISEASES OF THE NERVOUS SYSTEM. 

Neurasthenia. — When we consider what a large number of 
different organic and functional abnormalities go to make up the 
clinical picture of this condition it is not surprising to note that 
blood-pressure findings are inconstant. As has been described 
elsewhere, many of these cases belong in the category of "con- 
stitutional low arterial pressure" (q. v.), but some cases have been 
reported as associated with hypertension. Symptomatic improve- 
ment is generally attended by the reestablishment of a more normal 
pressure, whether this means a rise or fall. 1 "Neurasthenia" 
associated with high blood-pressure generally calls for a vision of 
diagnosis, which will not infrequently be changed to nephritis or 
cardiovascular hypertensive disease. 

"In true neurasthenia, in real exhaustion of the nervous centres 
from whatever cause arising, the blood-pressure is low, lower than 
in any other chronic malady, except the terminal phases of cancer 
tubercle and other wasting disease" (Leonard Williams). The 
effects of prolonged mental and physical strain and exhaustion 
as exemplified by soldiers returning from the battle front in France 
produces arterial hypotension. Montier reports that a well-marked 
fall in pressure occurs both in soldiers starting out with normal 
pressures and in those who do so with hypertension. 

Neuroses, etc. — In the neuroses are often found unequal radial 
pressure on the two sides as well as a general lability of pressure. 
These signs may be of use in diagnosticating between neurosis and 
simulation. 2 Pain produces a rise of blood-pressure and an increased 
pulse rate. Simulated pain does not. This fact has been turned 
to practical application in the detection of malingering in relation 
to industrial insurance. In persons with normal sensibility the 
blood-pressure under the application of faradic stimulation to the 
upper thigh rises from 8 to 15 mm. In organic affections of the 

1 Macnamara, Lancet, July 18, 1908. 

2 Sand, Les Anomalies de la Tension, Sanguine, etc., Arch, intern, de Med. Legale, 
1910, p. 349. 

24 



370 DISEASES OF THE NERVOUS SYSTEM 

spinal cord, multiple sclerosis, hysteria, etc., it remains unaffected 
when stimulation is applied to analgesic regions. 1 

If the systolic pressure is taken in one arm and simultaneously 
the diastolic pressure in the other (for celerity of procedure), and 
the subject is emotionally disturbed by conversation, gesture, or 
the application of ice to the abdomen, (1) marked variations of 
the maximum pressure are said to indicate abnormal stimulability ; 
(2) if the diastolic pressure meanwhile remains unaltered the 
vascular system is normal; (3) if the diastolic pressure shows 
sudden variations of over 15 per cent, of the systolic pressure we 
are dealing with arteriocapillary sclerosis. 2 Landerer found abnor- 
mal arteriocapillary pressure relations in neuroses. 

Peripheral Neuritis. — In the early stages of brachial neuritis, 
Stewart found the blood-flow greater than in the unaffected hand, 
a finding which he interpreted as indicating a partial paralysis of the 
vasoconstrictor fibers in the nerves involved. 

In neuritis affecting chiefly the muscular nerves, disturbances 
of the blood-flow were less conspicuous than when the cutaneous 
nerves were involved. This is presumably due to the fact that 
a large amount of the total blood-supply of the extremities traverses 
the skin of the parts. 

Cases of long-standing unilateral neuritis were found by Stewart 
to show a diminished blood-flow on the side affected, owing either 
to diminution of the arterial lumen following injury of the vasomotor 
nerves or perhaps to an adaptive correllation between diminished 
function and blood-supply. 

Mental Disease. — The reports on blood-pressure in abnormal 
psychic states are so variable and contradictory, and the range of 
abnormality so slight, that one cannot but feel that in the majority 
of cases at least no definite relationship exists. Xor is this surprising 
when we consider how greatly blood-pressure is normally affected 
by emotional disturbances. 

In simple, acute, passive, and demonstrative melancholia high 
pressures have been reported, whereas chronic melancholia is 
associated with hypotension. Hawley states that cases of mania 
show definite and typical blood-pressure changes — a large pulse 
amplitude with sudden pulsatory oscillations and an increased 
pressure. These phenomena disappear when the mental state again 

1 Curschmann, Deut. med. Woch., October 15, 1907. 

2 Schrumpf and Zabel, Die diagnostische Bedeutung der psychogenen Labilitat 
des Blutdruekes, Miinch. med. Woch., 1911, lviii, 1952. 



DEMENTIA PRECOX 371 

becomes normal. In pure senile mania and melancholia the readings 
correspond to those registered in the same states in earlier life. 
Senile dementia, characterized by restless fidgeting, etc., shows 
increased pressure. 1 In depressed and stuporous mental states 
low pressures are found. 2 

Dementia Precox. — According to Perazzolo 3 74 per cent, of 
these cases have a low blood-pressure. Turner found no definite 
relation between blood-pressure and either exalted or depressed 
mental states. The height of the pressure seemed mainly dependent 
upon the age of the patient and upon the presence of renal or 
cardiovascular complications. 4 

Epilepsy. — Epileptics not infrequently have a slow pulse rate, 
a low blood-pressure, and evidences of peripheral stasis. Russell, 5 
in his Goulstonian lecture, enumerated many interesting and 
suggestive points in an analogy between epileptic seizures and 
vascular spasm. We cannot, however, assume that such conditions 
affect the cerebral vessels in the same manner as or simultaneously 
with the peripheral arteries. Furthermore, there is still some 
difference of opinion as to whether the cerebral vessels possess 
vasomotor nerves. But the clinical picture of epilepsy presents 
many features which fit well into a hypothesis of vasomotor crises 
(aura, pallor, syncope, convulsions, etc.). 

Blood-pressure has been found to increase several hours before 
the attack begins. During the seizure it is said to rise still further 
(20 per cent.) and to fall after the attack; but often to remain 
somewhat elevated between paroxysms. 6 It has been shown that 
in many cases rhythmic blood-pressure variations occur which 
are not due to respiratory movements (Traube-Hering waves). 
Preceding the seizure (twenty-six to sixty seconds) there is a rise 
of pressure (followed in some cases by a sudden fall), then apnea, 
and finally the convulsion. 7 The pulse is variable. "A study of 
the changes in the respiratory and circulatory systems in some 

1 Alexander, Lancet, July 5, 1902. 

2 Hawley, Blood-pressure in States of Excitement and Depression, Arch. Int. Med., 
1913, xii, 526. 

3 Revista sperimentale di Freniatria, April 30, 1909. 

4 Turner, Observations on the Blood-pressure and Vascular Disease in the Female 
Insane, Jour. Ment. Sci., 1909, xlv, 419. 

6 Some Disorders of the Cerebral Circulation and Their Clinical Manifestations, 
Lancet. April 3, 1909, pp. 963, 1031, 1093. 

Lallemand and Rodiet, Des Modifications de la tension arterielle chez les epi- 
leptiques L'Encephale, iv, No. 11. 

7 Gibson, Good, and Penny, The Pulse Immediately Preceding the Epileptic 
Attack, Quarterly Jour. Med., 1910, iv, 1. The authors could find no alteration 
of the pulse amplitude up to the point of the seizure. 



372 DISEASES OF THE NERVOUS SYSTEM 

of the cases of epilepsy suggests that the site of the discharge is 
in the medulla and pons (the 'lowest level of fits' of Hughlings 
Jackson). Likewise it points to the medulla as participating in 
the discharge in all cases of epilepsy whether this discharge originates 
them or not." 1 

Brain Tumors, Hemorrhages, Meningitis, etc. — The increased 
intracranial tension which occurs in cases of apoplexy and brain 
tumor may be closely simulated experimentally. The symptoms 
of the two conditions as well as their mechanism is essentially 
similar. Sudden increase of intracranial tension produces an 
acute anemia of the brain, which, being enclosed within osseous 
confines, is relatively incompressible. The only possible relief 
from such compression can come through absorption of the cerebro- 
spinal fluid. If the rise in arterial tension is prevented death 
occurs from medullary anemia. 

With increasing compression the following symptoms generally 
occur in the order mentioned: (1) unconsciousness; (2) respiratory 
abnormalities; (3) increased arterial tension with bradycardia; (4) 
hypotension, tachycardia, death. Associated with these symptoms 
rhythmic fluctuations of blood-pressure (Traube-Hering waves) and 
Cheyne-Stokes respiration are apt to occur (see pages 41 and 290). 

The attendant rise of systemic blood-pressure is therefore com- 
pensatory; an effort to prevent medullary anemia, and if prevented 
causes death. The symptoms which arise are for the most part 
due not directly to pressure but to cerebral anemia. When intra- 
cranial pressure becomes sufficiently great certain symptoms and 
signs become apparent (headache, vertigo, vomiting, choked disk, 
etc.). If pressure is increased still further, bulbar symptoms 
develop: bradycardia, hypertension. Finally, if anemia threatens 
the vital centres life can only be maintained by a marked rise of 
general blood-pressure, and this at least intermittently usually 
occurs. Some of the highest blood-pressure readings on record 
(300 mm.+) have been encountered under these conditions. 
Eventually, unless the pressure is relieved, death occurs as a result 
of central and systemic exhaustion, preceded by a fall of tension 
and an increased pulse rate (see page 42). 

Any increase of the cerebrospinal pressure, whether due to tumor, 
softening, hemorrhagic meningitis, cerebral or cerebrospinal 
meningitis (serous or purulent) tends to cause a rise of systemic 
blood-pressure. Especially is this the case if the pressure is exerted 

1 Pollock and Treadway, A Study of the Respiration and Circulation in Epilepsy, 
Arch. Int. Med., 1913, xi, 445. 






APOPLEXY 373 

in the posterior cerebral fossa, causing a stimulation of the vaso- 
constrictor centre, and if the rise of intracranial pressure be rapid. 
Brain tumors are usually slow in growth and arterial hypertension, 
bradycardia and respiratory disturbances are not marked unless 
a sudden increase of intracranial tension occurs— hemorrhage, 
edema or ventricular effusion (Cushing). 

If the cerebrospinal pressure is relieved by lumbar puncture or 
trephining, blood-pressure falls, the bradycardia is replaced by 
a normal pulse rate and respiratory abnormalities disappear. 
There is often a distinct parallelism between the two pressures. 1 

From what has been stated it is evident that phlebotomy is 
generally contra-indicated in cases of cerebral hemorrhage. On the 
other hand, a progressively rising arterial pressure is often the most 
useful indication of an increase of hemorrhage and of consequent 
cerebral compression, and may therefore be used as a criterion as 
to whether an operation for decompression is or is not warranted. 

Apoplexy. — Immediately after an apoplexy, bradycardia with 
very high blood-pressure is sometimes seen. These symptoms result 
from increased intracranial pressure. The usual range of pressure 
"after a stroke" is between 150 and 200 mm., but normal pressures 
may be found, or higher pressures (300 mm.+) than are encountered 
in almost any other clinical condition. The value of pressure 
readings depends mainly upon a knowledge of the pressure which 
existed preceding the attack. It is more important to know 
the general trend of the pressure — whether upward or downward 
than actual figures. Thus a steadily rising pressure indicates 
cerebral compression and may call for decompression, whereas a 
steady fall points to vasomotor failure, which often leads to death. 
Blood-pressure readings may be of value in diagnosticating between 
apoplexy and embolism. High pressure is evidence in favor of the 
former, and low pressure of the latter. It appears, however, that 
apoplexy, even when associated with hypertension and chronic 
nephritis, is more commonly due to thrombosis with cerebral 
softening than to actual vascular rupture. Certainly this has been 
the case at the Philadelphia General Hospital. The importance of 
pressure exacerbations as induced by exercise in precipitating 
apoplexy has perhaps been overestimated, a considerable number 
of "strokes" occurring while the patients are at rest if not actually 
asleep, although, theoretically, increased pressure would tend to 
favor apoplexy or embolism, and decreased pressure thrombosis. 

1 Parisot, J., Hypertension cephalo-rachnidienne et pression arterielle, Compt. 
rend. Soc. biol., 1909, lxvi, 939. 



374 DISEASES OF THE NERVOUS SYSTEM 

The statement has been made that in cases of hemiplegia, due to 
thrombosis, the pulse is rapid, intermittent and of low tension, 
whereas hemorrhage produces hypertension and bradycardia. This 
appears to be true in typical cases. Often even rapidly fatal cases 
of hemorrhage fail to show either of the last-named symptoms 
(Collins) . 

Hemiplegia. — Pressure differences in corresponding extremities 
are not infrequently seen in cases of hemiplegia. Dana states 
that marked differences on the two sides of the body suggest involve- 
ment of the optic thalamus. 1 Stewart found an abolition of vascular 
reflexes in an old case of hemiplegia on the affected side (see page 
239). "In hemiplegia there is, in general, a marked deficiency in 
the blood-floiv in the paralyzed members. Considerable differences, 
however, exist in different cases in this regard, and also in the extent 
to which the vasomotor reflexes from the normal to the paralyzed 
part are affected. Whether these differences depend at all on the 
position of the lesion or are associated with the duration and com- 
pleteness of the paralysis has not been determined. There is some 
evidence that reflex vasoconstriction is more easily produced in the 
paralyzed parts than reflex vasodilatation." 2 

It has been shown experimentally that in dogs and cats there 
is a limitable region of the cortex, irritation of which causes a 
blood-pressure increase that is not coextensive with the motor 
zone, but is in cats situated more anteriorly. Irritation of this 
zone is sure to cause splanchnic constriction. It has been sug- 
gested, but as yet not demonstrated, that the pressor effects of 
certain cortical regions are limited in their action to certain regions 
of the body. The occurrence of unilateral differences in temperature 
and edema in hemiplegia when the secondary effects of muscular 
paralysis can be excluded, indicate that similar cortical pressor 
centres exist in man. 3 

Locomotor Ataxia. — The crises of locomotor ataxia have long 
been recognized as clinical manifestations of the disease. The 
etiologic part taken by the sympathetic nerve was explained by 
Duchenne. Putnam suggested that lesions of the sympathetic 
nerve might, owing to their influence on the vasomotor system, 
account for certain secretory abnormalities. The importance of 
vascular spasm in the genesis of the crisis has been chiefly cham- 

1 Dana, Jour. Am. Jour. Med. Assn., December 19, 1909. 

2 Stewart, G. N., Blood Flow in the Hands and Feet in certain Diseases of the Ner- 
vous System, Arch. Int. Med., 1915, xvi, 270. 

» Lewandowsky, W., and Weber, E., Blutdruck u. Hirnrinde, Med. Klinik, 1906, 
ii, 385. 



SYRINGOMYELIA 375 

pioned by Pal, who reported a number of cases in which the crises 
were associated with hypertension (in one case 240 mm. Hg.) and 
who regards the abdominal cramps as resulting from a spasm of 
the splanchnic arterioles, and a stretching of the nerve plexuses of 
the arterial wall. The attacks are sometimes relieved by nitrite 
of amyl. The rise of pressure occurs somewhat before the onset 
of pain, which begins when a certain variable high point is reached. 
The arteries become tense and the pulse rate increased. The 
pressure increase generally amounts to more than 50 per cent. 

Heitz and Norero 1 believe that the rise of pressure is the result 
of pain which they explain is due to a paroxysmal irritation of 
the posterior roots, and which is accompanied by local reflex 
phenomena in the corresponding segments; either (1) motor 
(vomiting, constipation) or (2) vasoconstrictor (hypertension). A 
rise of pressure is often absent in old cases owing to degeneration 
of the posterior roots, especially if chronic hypertension is associated. 
In opposition to Pal they failed to find arterial hypertension in cases 
of peripheral crises, although in most of their cases the disease was 
advanced. Stewart found the rate of blood-flow in both hands and 
feet diminished in tabes; together with feeble vasomotor reflexes. 

Paresis. — The early observations of blood-pressure in paresis 
made by Pilcz and Alexander showed hypotension. Craig found 
the tension high during mental depression and low during exaltation. 
The more recent studies of Walton 2 indicate that the average 
pressure in paresis is high, due doubtless to arteriosclerotic accom- 
paniments. When cardiac and renal diseases are excluded the 
pressure is slightly lower than normal. Such hypotension is, 
however, neither sufficiently great nor constant to be of diagnostic 
or prognostic value. The excited states are associated with variable 
pressures, but depression is more often accompanied by high than by 
low pressures. Toward the termination of the disease very marked 
hypotension may occur. 

Syringomyelia. — In a case of syringomyelia thermic stimulation 
of the affected arm produced no reaction in its fellow, whereas 
similar stimulation of the unaffected side arm produced a normal 
reaction on the diseased opposite side. These findings have been 
construed as showing that sensible stimuli occur in the "anti- 
dromal direction" after the manner of an axon reflex and produce 
a vasodilatation. 3 

1 De la pression arterielle chez les tabetiques, Arch. d. Mai. du Cceur, 1908, i, 505. 

2 The Blood-pressure in Paresis, Jour. Am. Med. Assn., 1906, xlviii, 1341. 

3 Hess, L., and v. Bergmann, E., Ueber Gefaessreflexe, Wien. klin. Woch., 1913, 
xxvi, 1297. 




CHAPTER XVII. 
BLOOD-PRESSURE IN SURGERY AND OBSTETRICS. 

The Effects of Hemorrhage. — When an artery of large size is 
torn or cut and the resultant hemorrhage is considerable, the 
diastolic pressure falls, as does also the systolic pressure, although 
to a lesser degree. The pulse pressure therefore increases and the 
left ventricle continues its normal output. Peripheral venous 
flow is, however, promptly reduced and soon the fall in venous 
pressure fails to supply an "effective" right auricular pressure. 
As a result of inadequate filling of the right heart, pressure falls 
in the pulmonary artery and in the left auricle, and systolic left 
ventricular output promptly falls. The medullary centres are 
stimulated by the decreased blood-flow, the pulse rate rises from 
depression of the cardio-inhibitory centre and vasoconstriction 
results from central stimulation. In addition to this mechanical 
factor chemical changes also produce their effects. The loss of 
erythrocytes from the blood-stream with its consequent reduction 
in the oxygen-carrying power of the blood, together with a slug- 
gish circulation in the peripheral capillaries, leads to a decrease in 
the volume per cent, of oxygen in first the venous, and later, the 
arterial blood, while the carbon-dioxid content of each remains un- 
changed. This reduction in the hematogenous oxygen content 
causes hyperpnea, which causes for the time being a better average 
auricular pressure. In brief, "the fall of arterial pressures is 
counteracted by the augmented breathing, an accelerated heart, 
an accommodative contraction of the larger vessels and by 
peripheral constriction leading to an increased resistance and 
diminished flow in spite of the reduction of viscosity." 1 

When hemorrhage ceases the loss of the blood bulk is made up 
by the absorption of lymph from the tissues. The rise of blood- 
pressure which results may be abetted by intravenous saline or 
salo-alkaline infusion. There appears to be no experimental evidence 
supporting the view generally held that active secondary, post- 
hemorrhagic vasoconstriction plays much of a part in this post- 
hemorrhagic rise of the mean pressure. 2 

The consecutive changes occurring during hemorrhage are 
represented in the following schemas taken from Wiggers's article. 

1 Wiggers, C. J., Modern Aspects of the Circulation in Health and Disease, Phila- 
delphia, 1915, p. 339. 

2 Wiggers, C. J., Pathologic Physiology of the Circulation during Hemorrhage, 
Arch. Int. Med., 1914, xiv, 33. 



THE EFFECTS OF HEMORRHAGE 



377 



SEQUENCE OF EVENTS DURING HEMORRHAGE. 
Reduction in Total Volume of Blood. 



/ 



\ 



Reduction in red cells and 
percentage of hemoglobin 



Venous blood-C02 unchanged 

decreased 

Arterial blood-C02 increased 

O2 decreased 



Reduction in total arterial resistance 

Decreased diastolic pressure 

i 
Increased systolic discharge of heart 

4 

Lower systolic, increased pulse-pressure 

i 

Decreased flow in peripheral veins 

J- 
Decreased right auricular pressure 

I 
Decreased output of right ventricle 

i 
Decreased pulmonary arterial pressure 
and left auricular pressure 

i 

Decreased output of left ventricle 

i 

Smaller pulse-pressure 

i 
Further fall in systolic and diastolic press- 
ures 

Decreased flow through medulla 

S I \ 

/ . 1 \ 

Stimulate Stimulates Depresses 

respiratory centre vasomotor card.-inhib. 

(deeper respirations) centre centre 

\ I • 

Reductions of red cells by ^\ Tend to counteract fall of pressure 

dilution of blood \ 

J \ / 

Decreased viscosity Tend to increase flow through small vessels 

SEQUENCE OF EVENTS DURING TERMINAL STAGES. 
Loss of Blood Volume Exceeds Resorption of Lymph. 
Red corpuscles reduced to minimum 
/ 



Stream slowed in tissues 

i 

Osmosis toward blood-stream 

i 

Increase in volume 



Oxygen percentage in arterial \ 
blood decreases 



Progressive increase in COa<- 



\ 
Systolic discharge diminishes due to lack 
of diastolic filling 

i 
Pulse-pressure progressively diminished 
\ I 

->Respiratory centre depressed 
I 
Heart depressed by anemia 

I 
Beats slower. Feebler 

1 
Respiratory periodic gasps 

1. 

Asphyxial conditions 

I 
Heart slow, large amplitude of contraction 

i 
Ventricular fibrillation, cessation 



378 BLOOD-PRESSURE IN SURGERY AND OBSTETRICS 

Blood-pressure readings should be made in all cases in which 
anesthetics or surgical procedures are employed before, if possible 
during, and after the operation. Arterial hypertension will often 
indicate the presence of renal disease when the routine urine ex- 
amination fails to reveal it. A fall of pressure during the course 
of the operation is one of the surest methods of detecting the begin- 
ning of shock, whether this occurs during or after the conclusion 
of the operation. A fall of pressure to below 100 mm. Hg., together 
with a rising pulse rate, is an indication for immediate treatment. 
Shock is at hand when the pulse pressure falls to 10 to 15 mm., 
or when the diastolic pressure falls to or below 70 mm. Hg. 
(McKeson). When possible the patient's normal pressure should 
be obtained the day before the operation, or at least not immedi- 
ately preceding it, because fear and excitement both tend to increase 
the systolic pressure, and the pulse rate. A steady pressure is the 
best indication of a satisfactory condition on the part of the patient. 
Fluctuations of tension point to exhaustion. Patients with marked 
hypertension (180 to 210 mm. Hg.) require special care. The 
possibility of apoplexy, uremia, or heart failure must be borne in 
mind, and yet such patients not infrequently make perfect recoveries. 
Blood-pressure readings alone cannot be used as a criterion of safety; 
the patient's general condition must be carefully considered. Cases 
of arterial hypotension, especially if this condition is associated 
with lymphocytosis and other evidences of status lymphaticus, 
withstand anesthesia as badly as they do infectious disease. 

"The practical surgeon should have knowledge of the following 
data: The effect of the general narcotic on blood-pressure and its 
relation to shock; whether in certain operations shock is less if 
the operation is carried on under spinal or local anesthesia, the 
effect of hemorrhage, the duration of the operation, exposure of 
the tissues to the air, effects of extreme heat or cold, the effect of 
manipulation or injury in various tissues or organs" (Bloodgood). 
While the manipulation of sensitive organs causes a primary rise 
of pressure, such a procedure may go far toward exhausting the 
vasomotor centre. 

Surgical Shock. — Surgical shock has been described as "a state 
of general apathy, reduced sensibility, extreme motor weakness, 
great pallor, very small pulse, thready soft arteries, irregular gasping 
respirations, and subnormal temperature." 1 There is perhaps no 

1 Meltzer, S. J., The Nature of Shock, Arch. Int. Med., July, 190S, p. 571. * 



SURGICAL SHOCK 379 

subject in the whole domain of surgery regarding the pathology 
of which more radical differences of opinion exist than shock. 
This is at least in part due to the fact the term shock is applied to 
various conditions which may arise from trauma, intoxications, 
hemorrhage, etc. It has been suggested (Mann) that the term 
"shock" (similarly to the much abused and too inclusive term of 
"rheumatism" should be dropped or if used at all, be limited to a 
condition in which without demonstrable hemorrhage, the amount 
of circulating fluid has been greatly diminished owing to venous or 
capillary stasis, or to exudation of serum or the diapedesis of cor- 
puscles. Since the publication of Crile's work on blood-pressure 
in relation to surgical shock, the view that this condition is the result 
of an exhaustion of the vasomotor centres has been widely accepted. 
Crile originally stated that " neither the heart muscle, nor the cardiac 
centres, nor the respiratory centre, are other than secondarily 
involved." 1 Collapse is due to a suspension of the function of the 
cardiac or of the vasomotor mechanism or to hemorrhage. These 
statements are based upon investigations of a large amount of 
clinical and experimental material which showed that (1) the only 
constant finding in cases of shock was a fall of blood-pressure; (2) 
there were no constant demonstrable lesions in the circulatory 
apparatus; (3) the fall of pressure was not due to exhaustion of the 
peripheral nerve vascular mechanism; (4) that cocainization or 
destruction of the vasomotor centres produces a fall of pressure to 
the shock level; (5) that drugs or other methods of treatment which 
raised arterial pressure were beneficial, whereas other stimulants 
which were employed were either useless or definitely detrimental. 
According to this hypothesis, then shock is due to an exhaustion 
of the vasomotor centre resulting from centripetal sensory stimuli. 

In shock we find the diastolic pressure decreased, the pulse rate 
and the pulse pressure increased. When cardiac exhaustion occurs 
the systolic pressure falls toward the diastolic level until the pulse 
pressure becomes so small that the cardiac and respiratory centres 
are no longer sufficiently supplied with blood and death occurs. 

"A respiratory rate of more than 30 per minute is too rapid to 
assist in moving the blood, thus throwing the whole burden upon 
the heart" (McKeson). 

The experiments of Porter 2 have shown conclusively that the 

1 (rile, G. W., Blood-pressure in Surgery, Philadelphia, 1903. 

2 The Relation of Afferent Impulses to the Vasomotor Centres, Am. Jour. Physiol., 
1910, xxvii, 276; and The Vasotonic and Vasoreflex Centre, ibid., 191.5, xxxvi, 418. 



380 BLOOD-PRESSURE IN SURGERY AND OBSTETRICS 

depression or fatigue of the vasomotor centre can no longer be 
considered as the primary cause of shock. Nor has it been demon- 
strated that the peripheral bloodvessels constantly or uniformly 
lose their tone. Mann 1 found that no amount of sensory stimulation 
would produce shock in the anesthetized animals so long as the 
abdomen is not opened, and hemorrhage is prevented. 

Based on more recent investigations, Crile 2 believes that the 
essential lesions of shock are in the brain cells and are caused by 
the conversion of potential energy in the brain cells into kinetic 
energy at the expense of certain chemical compounds stored in 
the cells. As a result of certain noci impulses (fear, exhaustion, 
anesthesia, insomnia, etc.) the brain threshold is lowered and the 
trauma of operation or injury may produce the shock. In order 
to avoid shock it is necessary to exclude these noci impulses both 
of the special senses and of common sensation. The technique of 
anoci-association consists briefly in excluding all psychic stimuli 
by proper preoperative care of the patient, protecting the brain 
against destructive psychic strain during the operation by complete 
anesthesia and preventing nerve trauma by blocking the nerves 
with local anesthetics. Crile lays the greatest stress on the psychic 
element, a conception which is not essentially at variance with 
Henderson's theory. 

Yandell Henderson, 3 on the other hand, believes that shock 
results from a lack of fluid in the circulation. According to this 
view there is a loss of C0 2 from the blood (acapnia) which results 
from increased respiration due to pain, trauma, fever, acidosis, 
exposure of tissues, or maladministration of the anesthetic. This 
causes a diminution of hemic osmotic tension, increased fluid 
transudation to the tissues, and a decrease in the total volume of 
blood. Owing to a fall of venous pressure the heart is no longer 
adequately filled with blood, and hence the systolic output dimin- 
ishes, and a condition analogous to hemorrhage ensues. The experi- 
ments of Morison and Hooker 4 indicate that loss of venous tone, 
causing a stagnation of blood in the veins and an insufficient filling 
of the right heart (as previously maintained by Henderson) plays 
a considerable part. Mann's investigations indicate that the loss 

1 The Peripheral Origin of Shock, Bull. Johns Hopkins Hosp., 1914, xxv, 205. 

2 The Kinetic Theory of Shock and its Prevention through Anoci-association 
(Shockless Operation), Lancet, July 5, 1913, p. 7. 

3 Amer. Jour. Physiol., 1910, xxvii, 167. 

4 The Vascular Tone and Distribution of the Blood in Surgical Shock, Am. Jour. 
Physiol., 1915, xxxvii, 86. 



SURGICAL SHOCK 381 

of serum and erythrocytes caused by handling of the delicate 
vascular area of the splanchnics plays an important role. 

Corbett's 1 experiments lead him to conclude that shock is of a 
composite nature, in which epinephrin exhaustion and oligemia are 
predominating factors, while anesthesia, pain, fright and trauma 
are immediate agents in producing epinephrin exhaustion as well 
as shock. Not "that epinephrin loss is shock, but rather epi- 
nephrin is necessary to overcome shock, and anything that 
depletes epinephrin favors the development of that condition." 
The foregoing hypotheses have aroused much discussion, and the 
true explanation must as yet be regarded as unsettled. Numerous 
other theories have been advanced and discussion has been in- 
conclusive. It appears agreed that " low blood-pressure is a constant 
accompaniment of shock, so constant, indeed, that investigators 
practically always express the state of shock in terms of manometric 
pressure." 2 For a more complete discussion the reader is referred 
to Parham's recent review of the subject. 3 

In the early stages of shock a marked rise of pressure often occurs 
as the result of stimuli which exert a vasoconstrictor influence, but 
owing to continuous stimulation of this kind a stage of depression 
occurs which may result in death. 

Hemorrhage is an important contributing factor in the produc- 
tion of shock, and all avoidable bleeding should be promptly 
checked. Sudden or large hemorrhage manifests itself by a fall of 
blood-pressure. A rapid and persistent fall of pressure with an 
increased pulse rate often indicates a loss of blood too great for the 
organism to compensate for by peripheral vasoconstriction and by 
an additional expenditure of cardiac energy. The diastolic pressure 
is an index of far greater importance than the systolic, and a 
diastolic pressure of 50 mm. seems to be the lowest pressure 
at which the circulation can be maintained. (See Hemorrhage, 
p. 376. ) 4 Rough manipulation, tearing of the tissues, espe- 
cially when these have a large afferent nerve supply, must be 
avoided. "During the operation the amount of anesthetic 

1 The Suprarenal Gland in Shock, Jour. Am. Med. Assn., 1915, lxv, 380. 

2 Gray and Parsons, Anis and Gale Lectures, Royal College of Surgeons of London, 
March, 1912, British Med. Jour., April and May, 1912. 

3 Parham, F. W., Shock, Its Nature and Management, South. Med. Jour., 1913, 
vi, 763; see also, The Present Status of Our Knowledge of Shock, J. M. "Wainwright," 
Penn. Med. Jour., December, 1914, p. 180; and Anesthesia, Gwathmey, New York, 
1914. 

4 Balard, B., La Tension Arterielle Minima Element de Prognostic des Hemor- 
rhagies Graves de la Grossesse, Arch. Mens. d'Obst. et de Gyn., 1914, iii, 241. 



382 BLOOD-PRESSURE IN SURGERY AND OBSTETRICS 

should be as small as possible, the operation should be per- 
formed as quickly as is compatible with the safety of the patient 
and the purpose of the intervention; tissues should be handled 
as gently as possible; if large nerves must be divided, as in amputa- 
tions, they should be blocked with cocain injection; tissues should 
be exposed to air only when absolutely necessary; they should 
be protected with warm, moist gauze; the patient should not be 
exposed to extremes of heat or cold. The weaker the patient to 
be subjected to operation, the more attention must be given to these 
details which lessen shock." 1 Complicating factors such as anemia, 
nephritis, diabetes, alcoholism, acute and chronic infections, 
metabolic disturbances, and psychic factors must also be borne 
in mind. 

The handling of tissues and organs supplied with sensory nerves 
by the cerebrospinal system is more apt to induce shock than is 
the manipulation of those whose nerve supply is derived from the 
sympathetic nerves or the lower vagus. Furthermore, inflammation 
enhances the sensibility. Tumors are said to be insensible, but their 
connection with other tissues must be borne in mind. 

The Treatment of Shock. — The keynote of treatment lies in 
prevention which has already been considered. The arterioles 
once they are relaxed, do not readily regain the tonus. Hence the 
pressure required to keep up the circulation in the medulla and in 
the coronary arteries must be produced by increased cardiac work. 
Drugs are for the most part unsatisfactory. The most rational 
therapeusis, however, consists in the slow and prolonged intra- 
venous administration of pituitrin or epinephrin in normal salt 
solution. The amount of infusion necessary may be gauged by 
blood-pressure readings. Recent researches have shown that the 
intravenous administration of a molecular (8.-± per cent.) solution 
of sodium bicarbonate produces a marked rise of blood-pressure, 
an increased cardiac amplitude, and depth of respiration. These 
effects are due mainly to alkalinity, much less to bulk and hyper- 
tonicity, and in part to some other undetermined factor acting 
chiefly upon the heart, but not to the increased carbon dioxid 
content of the blood. 2 Investigations have shown that in shocked 
animals camphor, administered intravenously, causes an actual 
fall of blood-pressure. It is more apt. to be efficacious when given 

1 Bloodgood, J. C, Surgical Shock, American Practice of Surgery. Bryant and 
Buck, 1906, i, 469. 

2 Scclig, Tierney. and Rodenbaugh, Jour. Am. Med. Assn., 1913, lx, 23*. 



SURGICAL SHOCK 383 

subcutaneously. Strychnin likewise does not raise blood -pressure, 
although it may be useful on account of its stimulation of the 
nerve centres. Nitroglycerin is definitely contra-indicated, although 
it may temporarily give a better color to the skin. Strophanti! in, 
intravenously increases pressure and is often useful. Cajfein 
intravenously tends rather to lower than to raise blood-pressure. 
Atropin when the skin is clammy is often useful. 

Inversion of the patient to increase blood-pressure in the brain 
may be tried, but not of course if the patient has already been in 
the Trendelenburg position. This posture may cause arhythmia 
and, according to Pope, 1 even heart block, "due either to acute 
dilatation, to toxins, or fatigue, or sepsis, or coronary clots, or 
direct trauma to some area of cardiac reflex." "It is quite possible, 
however, that from this position slight edema or exudate into the 
fourth ventricle may occur and may disturb the respiratory and 
pneumogastric centres. In shock from this cause, Pope suggests 
venesection from the jugular vein, cardiac massage and epinephrin 
in Ringer's solution forced backward in the arterial stream, as 
giving the only possible chance for recovery." 2 Atropin, strychnin, 
or caffein in hypodermic administration are currently employed. 
The patient's head should be kept low, the feet elevated, the body 
warm and quiet. Blood-pressure may be elevated by bandaging 
the extremities. Fresh air should be supplied and carbon dioxid 
in 6 per cent, concentration may be tried. 

According to Crile's anoci hypothesis, 3 stimulants are contra- 
indicated, while morphin and other sedatives may prove useful. 
Normal saline is beneficial temporarily and within limits, while 
human blood may be expected to yield the best results. All author- 
ities are agreed that preventive measures are of the greatest importance. 
The elimination to the greatest possible extent, of fear and anxiety 
on the part of the patient before, and in preparation for an operation 
is of the utmost importance. For this purpose a hypodermic 
injection of morphin before the patient is anesthetized is often most 
beneficial. With the same object in view the patient should see 
and hear as little as possible of the operating room and of the 
preparations which are being made for the impending operation. 

The Posture of the Patient. — The posture of the patient during 
operations of necessity entails marked changes in blood-pressure 

1 California State Jour. Med., December, 1913, p. 499. 

2 Edit. Jour. Am. Med. Assn., 1914, lxii, 776. 

3 Crile & Lower, Anoci-association, Philadelphia, 1914. 



384 BLOOD-PRESSURE IN SURGERY AND OBSTETRICS 

and blood distribution, with which the heart under the benumbing 
influence of anesthesia or if handicapped by disease, may be unable 
to cope. Thus in the morphinized animal carotid pressure falls 
owing to this effect of gravity in the head-up posture, and rises 
when the feet are uppermost. Compensation is established by 
cardiac and vasomotor reactions in the stronger animals, but 
rabbits die if the feet-down position is long maintained (fifteen 
minutes to two hours) from cerebral anemia, due to splanchnic 
dilatation which can no longer be overcome by respiratory move- 
ments (abdominal compression and diaphragmatic suction). The 
normal vasomotor tone is depressed by ether, and specially so by 
chloroform. Again, dogs may be killed by a prolonged Trendelen- 
burg position plus ether (not morphiri) anesthesia, the death 
resulting from failure of respiration, the heart action remaining 
good and the blood-pressure high. While death may occur similarly 
in the horizontal position, partial or complete respiratory faliure 
is more common in the head-down posture. 

Recent researches indicate that "the Trendelenburg -position is 
harmless for patients with normal hearts, provided that respiration 
is free and unobstructed." This "position should be used only 
with extreme caution in cases of cardiac disease." The position 
should not be established or relinquished suddenly. Using this 
posture forces a large amount of venous blood toward the heart, 
and, if this organ is capable of handling it, produces temporarily 
a marked increase of brachial blood-pressure. If the position is 
suddenly abandoned the venous pressure, and consequently the 
arterial pressure, fall and bulbar anemia may result, especially 
if vascular tone is depressed. 

Struggling, and pressure upon the abdomen by gauze pads, ban- 
dages, etc., may cause cardiac dilatation. The administration of 
morphin in moderate doses preceding the administration of ether 
is often advisable. It diminishes the amount of ether required, 
tends to prevent struggling, excitement, and acapnia, and does 
not in man impair vasomotor tone. Patients with heart disease, 
pneumonia, or empyema should be anesthetized gradually, in the 
sitting or semirecumbent posture (Gatch, Gann, and Mann). 1 

The Effect of Chilling during Anesthesia.— Under ether anesthesia 
the application of cold to dogs produces a marked rise of blood- 
pressure; under chloroform no such rise occurs. It seems, therefore, 

1 The Danger and Prevention of Severe Cardiac Strain during Ether Anesthesia, 
Jour. Am. Med. Assn.. 1913, lx, 1273. 



VISCERAL MANIPULATION 385 

that the narcotic dose of ether does not abolish vasomotor reflexes 
as does chloroform. The rise of pressure in the former instance 
causes a congestion of the internal viscera, a condition comparable 
to what occurs during the act of "catching cold," and probably 
accounts for the greater frequency of respiratory infections afterether. 1 

Visceral Manipulation. — Blood-pressure observations have taught 
the importance of avoiding, or at least minimizing, certain surgical 
manipulations. Thus a marked fall of pressure is caused by irrita- 
tion of the dura and of the subdiaphragmatic peritoneum, traction 
upon bloodvessels or nerves, renal or mesenteric vessels, the brachial 
plexus, or the testicles; by rough sponging, blunt dissection, exposure 
or rough handling of viscera, peritoneal flushing, separating ad- 
hesions, delivering tumors, extirpation of the kidney, exposure of the 
spinal cord, section of large nerve trunks unless previously cocainized. 
The upper portion of the peritoneal cavity is more sensitive than 
the lower. 

On the other hand, blood-pressure rises during divulsion of the 
sphincter ani and in stretching of the sciatic nerve. 

The following procedures produce but slight blood-pressure 
changes: incision of the scalp, chiselling of bone, separation of 
the periosteum, hernia operations (without adhesions), the resection 
of ribs, appendectomy (simple), incision of the kidney. Dragging 
upon the mesentery produces a much greater fall of pressure than 
handling the omentum. Especial care should be exercised in the 
region of the duodenum, pylorus and gall-bladder, owing to the 
possibility of interfering with the circulation in the larger venous 
trunks. Trauma to the pelvic viscera, on the other hand, has much 
less tendency to produce shock (Gatch). Under normal circum- 
stances the diaphragm materially aids the circulation by alternately 
increasing the pressure in the thoracic and in the abdominal cavities. 
But once the abdomen is opened, the diaphragm no longer increases 
intra-abdominal pressure during inspiration and hence less blood 
reaches the right heart. 

Concussion of the brain produces a fall of blood-pressure, com- 
pression, a rise (see page 372), but severe experimental injury of the 
cerebral hemispheres under complete anesthesia does not cause 
a fall of pressure. " Collapse from interference with the medullary 
centres is of course not true surgical shock" (Crile). 

1 Stursberg, Das Verhalten d. Blutdrucks unter d. Einwirk. v. Temperaturreizen 
in Aether u. Chloroform Narkose., Mitt. a. d. Grenzgeb. d. Med. u. Chir., 1910, 
xxii, 1. 

25 



386 BLOOD-PRESSURE IN SURGERY AND OBSTETRICS 

Manipulations of the Thoracic Viscera. — The effects of various 
surgical manipulations upon the blood-pressure, pulse rate, and 
respiration have been made by Flint. 1 

The detailed results cannot be given here, but the conclusions 
reached show that "the reactions of the medullary centres to 
operative traumatism as shown in these experiments suggest that 
we should be cautious in the treatment of the parietal pleura, 
particularly in tearing it at the angles of the intercostal wound by 
injudicious application of the rib-spreader. The lungs may be 
handled freely, but manipulations that tend to transmit traction 
to the great vessels and bronchi at the root of the lung should be 
reduced to a minimum. In heart suture the Sauerbruch method 
of temporary hemostasis leads to too serious a fall in blood-pressure 
to be safe except where other means of hemostasis fail. Any 
mechanical stimulation of the heart, either directly or through the 
pericardium, during suture, should be avoided as far as possible. 
Furthermore, in packing off the lungs to obtain an exposure of 
other thoracic viscera it would be wise to avoid any unnecessary 
trauma which might tend to reduce the blood-pressure excessively. 
These are the stimuli which, in the present set of experiments, 
have produced the most serious reactions." 

Manipulation of the Pelvic Viscera. — Manipulation of the pelvic 
organs during laparotomies may produce either a rise or a fall of 
pressure, depending upon the manner in which the viscera are 
handled. Experimental irritation of the genital mucous membrane 
(in dogs) produces a fall of pressure ranging between 5 and 50 
per cent. The fall of pressure is more marked if the stimulation 
is applied in the lower vagina; in the upper portion a rise of pressure 
may result. Irritation of the rectal mucosa causes a fall of pressure. 2 

Schroder found that manipulations of the female generative 
organs by way of the vagina caused less lowering of pressure than 
when a laparotomy was performed; but Crile found that manipu- 
lation always produced a rise which was proportional to the 
traumatism. 

Aspiration of the Pleura. — Vertigo, syncope, and even death may 
follow the withdrawal of fluid from the pleural cavity. It has been 
shown that these effects are not merely the result of altered pressure 

1 Flint, J. M., Physiologic Basis of Thoracic Surgery, Jour. Am. Med. Assn., 
1912, lix, 760. 

2 Belfield, W. J., Ueber depressonsche Reflexe, erzengt durch Schlehnhautreitzung, 
Arch. f. Anat. u. Phys., 1882, p. 298. 



PARACENTESIS ABDOMINALIS 387 

relations in the thorax, but that they are due to a depressor reflex 
originating in the pleura, which may be: (1) A central reflex cardio- 
inhibitory type, in which the heart is slow, intermittent, and there 
are great variations in the systolic and diastolic pressures, asso- 
ciated with slow respirations. (2) A vasomotor type showing a 
steady rapid decline of pressure without any great difference 
between the systolic and the diastolic readings. Respirations are 
shallow, sometimes rapid. This type, in contradistinction to the 
first, not infrequently terminates in death. The reflex may be either 
central or peripheral. To minimize the likelihood of these accidents 
care should be taken to avoid irritating the pleura with the trocar 
or drainage tube. 1 In seven out of eight pleural aspirations Clark 
found a fall of venous pressure (see page 141). 

Paracentesis Abdominalis. — This procedure is attended with 
much the same blood-pressure changes as those which occur when 
the pleura is aspirated. As might be expected a greater fall (32 
mm. on the average) occurs. 

"Up. to a certain point the general arterial pressure increases 
with an increase in the pressure of intra-abdominal fluid; beyond 
this point the blood-pressure falls. Quirin attributes the early 
rise in blood-pressure to increased resistance by compression to 
the flow of blood through the abdominal arteries; the fall occurs 
when the heart, handicapped by a diminished supply of venous 
blood, is no longer able to overcome the resistance of the abdominal 
arteries. Ascitic fluids have an intra-abdominal pressure of 19 
to 42 mm. Hg., according to Quincke. Quirin found that the 
intra-abdominal pressure fell 10 to 14 mm. after tapping, and that 
this corresponded with the simultaneous fall in arterial pressure 
of 5 to 10 mm. Hg. after paracentesis in four cases. Cook and 
Briggs record one case of abdominal paracentesis in which the 
pressure fell 35 mm. Hg. during the withdrawal." 2 

The rate of withdrawal is apparently more important than the 
amount so far as the immediate pressure is concerned. The ultimate 
pressure depends more upon the quantity of fluid withdrawn. 
External abdominal pressure favors a rise of pressure, as does 
also the recumbent posture. "Improvement is most pronounced 



1 Capps and Lewis, Blood-pressure Lowering Reflexes, Amer. Jour. Med. Sei., 
1907, exxxiv, 868. 

2 Capps, J. A., Some Observations on the Effect on the Blood-pressure of the 
Withdrawal of Fluid from the Thorax and Abdomen, Jour. Am. Med. Assn., January 
5, 1907, xlviii. 



388 BLOOD-PRESSURE IN SURGERY AND OBSTETRICS 

in those cases that undergo a marked fall in pressure during the 
operation" (Capps). 

The emotional disturbance entailed by a prospective operation, 
as well as the actual pain of puncture, produce a temporary eleva- 
tion of blood-pressure (see under Abdominal Distention and Blood- 
pressure, page 260). 

The majority of surgeons seem to be impressed with the impor- 
tance of blood-pressure readings in brain surgery. Horsley states 
that 25 per cent, of the sudden deaths after prolonged operations 
may be avoided by frequent observations. 

Drainage of the Bladder. — Drainage of the bladder, either by 
suprapubic incision or by a retained catheter as a preliminary 
procedure to prostatectomy, definitely lowers blood-pressure (aver- 
age in 50 cases, 166 to 145 mm.) and diminishes mortality. 1 

Anesthetics. — Anesthetics differ in their effect upon blood- 
pressure, and the degree to which a given drug lowers pressure is 
an index of the danger with which its administration is associated. 

Ether. — The early stages of ether anesthesia are associated with 
an increased blood-pressure due to psychic stimuli and muscular 
effort. This increased pressure is maintained through stimulation 
of the respiratory centre. Recent experimental evidence has shown 
that ether alone, even when employed in large amounts, rarely 
produces much depression of blood-pressure. 2 When anesthesia 
is complete the pulse rate and the blood-pressure are practically 
normal. A slight postanesthetic rise is often observed, which the 
administration of oxygen generally increases. During ether-oxygen 
anesthesia blood-pressure is invariably increased. If ether is ad- 
ministered intravenously a preliminary use of pressure (6-25 mm.) 
occurs to be followed at the end of from one to three hours by a 
fall of like degree (Honan and Hassler). Since ether is excreted 
by the stomach and reabsorbed, it has been found that the introduc- 
tion of olive oil into the stomach by means of a catheter before the 
patient has regained consciousness binds the ether and prevents 
or lessens reabsorption in the gastro-intestinal tract (E. Graham). 
A fall of pressure during anesthesia may result primarily from either 
vasomotor or from cardiac failure. Henderson 3 believes that both 
conditions are fundamentally due to acapnia resulting from excessive 

' Balfour, D. C, Mayo Clinics, 1913, p. 73. 

2 Guy, W., Goodall, A., Reid, H. S., Blood-pressure in Anesthesia, Edinburgh 
Med. Jour., 1911, n. s., iii, 126. 

3 Primary Heart Failure in Normal Subjects under Ether, Surg.. Gynec. and 
Obstet., 1911, p. 161. 



ANESTHETICS 389 

pulmonary ventilation in the stage of excitement. Prolonged 
ether-chloroform narcosis in rabbits is said to produce injury to 
the chromaffin system (Schur and Wiesel). 

The effect of morphin and ether anesthesia combined differs 
from that of ether alone. In the latter instance sensory stimuli 
are not completely blocked, although the sensorium is abolished and 
surgical anesthesia may be sufficient. 

Chloroform. — Blood-pressure is often reduced even in the earlier 
stages; under full anesthesia a marked fall is often present which 
in fatal cases continues progressively until death occurs, due to 
cardiac depression. Even in the earlier stages, however, the heart 
may temporarily cease contracting, owing apparently to reflex 
inhibitory stimuli originating in the air passages. In case of a 
diseased heart the arrest may be permanent. The depressant 
action of chloroform upon the heart is much greater than that of 
ether. Regarding the primary vascular effect of chloroform there 
is still divergence of opinion. Some investigations show an initial 
rise of pressure due to stimulation of the vasomotor centre. This 
stimulation does not increase blood-pressure, as it is more than 
counterbalanced by cardiac weakness (Cushny). Unlike ether, 
chloroform does not have any compensatory stimulating action 
to mask the effects of peripheral stimulation; it is this property 
which constitutes its danger (G. Miiller). If oxygen is combined 
with chloroform blood-pressure is much less reduced than by 
chloroform alone. 

Ethyl Chlorid. — The effect of ethyl chlorid upon the heart muscle, 
similarly to that of chloroform, is depressive, but nineteen times 
more of the former is required to produce similar results. Ethyl 
chlorid causes local peripheral dilatation. Vagus inhibition of the 
heart occurs readily. In concentration of from 10 to 20 per cent, 
a fall of blood-pressure results from vagus stimulation. If 30 per 
cent, or more is used, blood-pressure falls from cardiac muscular 
depression, although this is not so pronounced as after chloroform. 1 
Ethyl chlorid generally slows the pulse and produces a fall of blood- 
pressure. 2 It is by many regarded as a dangerous anesthetic, far 
inferior to nitrous oxid. 

Nitrous Oxid. — The administration of this drug is attended with 
a slowing of the pulse and a marked rise of arterial pressure. These 

1 Embley, Proc. Royal Soc, 1906, Lancet, April 20, 1907, Pharm. Jour., xxiv, 650. 

2 McCardie, The Position of and Mortality from Ethyl Chlorid as a General Anes- 
thetic, British Med. Jour., March 17, 1906, p. 616. 



390 BLOOD-PRESSURE IN SURGERY AND OBSTETRICS 

effects have been attributed both to a specific action and to the 
asphyxial condition of the blood. In arteriosclerosis, especially if 
associated with hypertension, it may cause vascular rupture. Crile 
states that " under approximately equal trauma the changes in 
the brain cells were approximately three times as great under 
ether anesthesia as under nitrous oxid anesthesia; that the fall 
in the blood-pressure was on the average two and a half times 
greater under ether than under nitrous oxid; and finally, that the 
condition of the animal was better after trauma under nitrous 
oxid than after equal trauma under ether." Bloodgood's experi- 
ence with nitrous oxid and oxygen anesthesia, even in cases of 
arterial hypertension, has been most favorable. 

Cocain. — Cocain stimulates the heart muscle directly or as the 
result of accelerator influence. In the early stages of intoxica- 
tion there is peripheral vasoconstriction (local action and central 
stimulation) causing a rise of blood-pressure. Later, pressure falls 
owing to peripheral action. Cocain has been almost entirely 
supplanted by the less toxic drugs, stovain and novocain, the 
former being used for spinal and the latter for local anesthesia. 

The subject of anesthesia cannot, of course, receive prolonged 
consideration here, but a few points may be emphasized. There 
seems to be no valid reason for chloroform as a substitute for ether 
in major operations. It should never be administered after a 
preceding period of ether excitement. For minor operations nitrous 
oxid is preferable. In using ether the subject should be quickly 
narcotized and kept "well under." Struggling during the adminis- 
tration and incomplete anesthesia are dangerous. The beneficial 
effects of rebreathing (CO2 stimulation) in preventing shock, as 
shown by Gatch, lend strong support to Henderson's explanation 
of this condition as resulting from acapnia. The preliminary 
administration of morphin is often desirable. Nitrous oxid with 
oxygen is for short operations an excellent anesthetic. 

The Cerebrospinal Fluid and Blood-pressure. — The normal 
pressure of the cerebrospinal fluid ranges between 60 and 100 mm. 
H 2 0. It may be increased to 200-800 mm. in meningitis or brain 
tumor. It should never be reduced below 60 mm. H 2 0. It varies 
and is practically identical with the pressure in the venous sinuses. 1 
A relatively small increase in cerebrospinal pressure stimulates 
the vasomotor, cardio-inhibitory and respiratory centres. When 

1 Frazier and Peet, Factors of Influence in the Origin and Circulation of the 
Cerebrospinal Fluid, Am. Jour. Physiol., 1914, p. 1018. 



CEREBROSPINAL FLUID AND BLOOD-PRESSURE 391 

pressure is increased considerably above the normal arterial pressure, 
respiration ceases, and there is an enormous rise of arterial pressure 
with a slow pulse. When the cardio-inhibitory centre becomes 
exhausted, blood-pressure rises still higher owing to the continued 
activity of the vasomotor centre, until the latter becomes par- 
alyzed, 1 whereupon blood-pressure falls. 

Lumbar Puncture. — Blood-pressure is the most valuable guide 
during this procedure. A well-marked fall of tension indicates 
immediate cessation. Lumbar puncture is sometimes followed by 
sudden syncope, especially when medicinal substances are injected. 
This may result from (1) the puncture of the dura — a rare but 
possible reflex disturbance; (2) increased intraspinal pressure; (3) 
the introduction of chemicals used for purposes of medication or 
for the preservation of sera. Auer's researches indicate that 
tricresol, which is used for the last-named purpose, causes a greater 
fall of blood-pressure than chloroform or formalin. 

"1. The puncture of the skin is accompanied by a rise in blood- 
pressure which varies in extent with the degree of consciousness, 
the pain, and the disturbance produced by the operation, but which 
is not accounted for entirely by these factors. Puncture of the 
dura causes a much larger rise, which is due not to pain or the 
disturbance produced but to a definite effect on the vasomotor 
centre. Similar rises occur in dogs under full anesthesia. 

"2. Withdrawal of cerebrospinal fluid per se tends to lower the 
blood-pressure, but the net result of lumbar puncture is to raise it 
for at least twenty minutes afterward. 

"3. The type of blood-pressure chart obtained in lumbar punc- 
ture, when the increased intracranial pressure is of subtentorial 
origin, is the same as that obtained in normal individuals; or 
as that obtained when the increased pressure is of supratentorial 
origin; but in the subtentorial types the variations are less pro- 
nounced. In subtentorial cases the rise is more sustained." 2 Blood- 
pressure readings should always be made during intraspinous 
medication. Berghausen 3 suggests that the needle be left in situ 
until blood-pressure returns to the same height as that at which it 
was preceding the spinal puncture. This seems hardly necessary 
if the serum has been given by the gravity method. According to 

1 Dixon and Halliburton, The Cerebrospinal Fluid, Jour. Physiol., 1914, xlviii. 317. 

2 Gray, H. T., and Parsons, L., Blood-pressure Variations Associated with Lumbar 
Puncture and the Induction of Spinal Anesthesia, Quart. Jour. Med., 1911-12, v, 339. 

3 Intraspinous Medication, New York Med. Jour., 1914, c, 1006. 



392 BLOOD-PRESSURE IN SURGERY AND OBSTETRICS 

the last-named author, sudden respiratory changes follow only 
when blood-pressure change has been marked — usually after a 
fall of pressure (see Meningitis) . If collapse symptoms occur, the 
head should be lowered, the feet elevated, and ether and strychnin 
should be given hypodermically. 

Spinal Anesthesia. — "1. Blood-pressure records from cases of 
high spinal anesthesia show at the outset an abnormally high 
blood-pressure due to mental anxiety; then a rise following lumbar 
puncture; next a 'preliminary fall,' followed by a further more 
marked 'main fall' as the paralysis affects the thorax. Finally, as 
the paralysis passes off, the blood-pressure rises to its original 
values. The 'preliminary fall' is due to: 

" (a) Flaccid paralysis of the abdominal and skeletal muscles. 
" (b) Subsidence of the disturbance caused by lumbar puncture. 
" (c) Onset of mental calm, amounting possibly to sleep. 

"The 'main fall' is due to the thoracic paralysis, which is not 
compensated for by overaction of the diaphragm, and consequently 
the aspiratory action of the thorax is diminished. 

"2. Marked deviations from this common type of chart are 
due to: 

" (a) Voluntary inspirations by the accessory respiratory muscles, 
and 

" (b) To a lesser extent by the activity of the higher centres. 

"Variations in the pulse rate do not closely follow those of the 
blood-pressure, but a certain degree of resemblance is often seen 
owing to the consciousness of the patient. 

" 3. Vomiting during spinal anesthesia is due to thoracic paralysis, 
which induces either: 

"(a) Anemia of the medulla. 

"(b) Excessive action of the diaphragm, which interferes with 
the stomach. 

"4. Blood-pressure records from cases of low spinal anesthesia 
show the ' preliminary fall' but not the ' main fall.' The ' preliminary 
fall' in these cases is due to: 

" (a) Subsidence of the disturbance caused by lumbar puncture. 

" (b) Onset of mental calm. 

" (c) In some cases from the degree of flaccidity of the abdominal 
muscles. 

"5. In the supine position there is no stagnation of blood in the 
great vessels, even when a very high spinal anesthesia is induced." 

Inasmuch as the normal blood-pressure depends upon afferent 



HEMOSTASIS BY BELT CONSTRICTION 393 

and efferent pressor and depressor stimuli it is evident that serious 
results may follow the cutting off of such impulses. A cessation 
of pressor impulses, for instance, would leave the effect of depressor 
fibers in predominance. 

The question of blood-pressure in spinal anesthesia is a complex 
one, owing to the physiologic action of the substances employed. 
In fifty cases studied by Mori the results were very variable, owing, 
it seemed, to the inconstant effects of cocain, epinephrin, and the 
patient's psychic state. 1 George Miiller, in Frazier's Clinic at the 
University of Pennsylvania, found that lumbar puncture caused 
a marked elevation of the blood-pressure not due to the pain, 
because it occurs even under anesthesia. In correct spinal anesthesia 
the complete block of peripheral impulses makes the pressure curve 
independent of the nature of the operation. If the anesthesia is 
allowed to extend upward it cuts off the pressor stimuli to the 
splanchnic area and may produce the effect of shock, or if it extends 
still farther upward, respiratory embarrassment or even paralysis 
may occur (see page 331). Smith 2 states that blood-pressure can 
be as profoundly lowered by spinal anesthesia as by section of the 
cervical cord. The greatest fall occurs when injections are made 
in the thoracic region, at which point the splanchnic vasomotor 
fibers are given off. This part of the vasomotor mechanism is 
first affected when injections are made in the lumbar region. It 
appears that diffusion of the drug depends greatly upon the bulk 
of the injection — the more fluid injected, the greater the diffusion. 
The most pronounced effects on blood-pressure occur when epi- 
nephrin was used in conjunction with novocain. Efforts to raise 
the fallen pressure by the intravenous infusion of epinephrin and 
pituitrin result in only a transient rise. 

Hemostasis by Belt Constriction (Momburg). — As a means of 
checking hemorrhage after severe trauma, in obstetrics, etc., with 
certainty, without an assistant and without the danger of local 
wound infection, Momburg has suggested winding a rubber tube 
tightly around the waist, one turn after another, until the femoral 
pulse disappears. This procedure, which causes a sudden rise of 
blood-pressure and which throws a corresponding burden upon 
the heart, should not be emplojed in case of cardiovascular disease. 

1 Mori, M., Das Verhalten des Blutdruckes bei Lumbalaniisthesie, Deut. Ztschr. 
f. Chir., 1904, lxxiv, 173. 

2 Blood-pressure in Spinal Anesthesia, Boston Med. and Surjr. Jour., 1915, cxxiii, 
502. 



394 BLOOD-PRESSURE IN SURGERY AND OBSTETRICS 

The suddenness of the cardiac strain may be somewhat mitigated 
by preliminary constriction of the thighs. It is absolutely essential 
that the constriction be very gradually relieved so that vasomotor 
tone and the distribution of blood may be gradually reestablished. 
It should never be applied in the case of elderly or obese women. 
Numerous accidents have occurred from defective technique. 
This procedure has not met with any practical acceptance, and is 
by many authorities condemned as a dangerous and unjustifiable 
procedure. 

Abdominal Conditions. — Blood-pressure readings may be of diag- 
nostic value in abdominal lesions. Thus unilateral suppurative 
renal disease causes a rise of pressure which falls after evacuation 
or extirpation. 1 Readings are of value in the diagnosis in visceral 
rupture, ectopic pregnancy, gastric or intestinal perforation, etc., 
all of which conditions cause a sudden and often marked fall of 
pressure. As a rule the extent of the fall depends upon the patient, 
the size of the perforation, the coexistence of hemorrhage, the 
presence of localizing adhesions, and the portion of the peritoneum 
involved. The larger the perforation, the less it is walled off; 
the greater the associated hemorrhage and the higher its location, 
the more will arterial pressure fall. The pain which often precedes 
or is associated with perforation causes a preliminary rise of pressure. 
Pressure readings naturally have a much greater value if the 
patient's normal pressure is known. Hence the value of routine 
pressure records. It is impossible to give any rules based upon 
absolute figures, but a systolic pressure below 90 mm. Hg. in asso- 
ciation with other signs would point to hemorrhage or perforation 
even in toxic patients prostrated by typhoid fever (see page 206). 
Acute inflammatory lesions in the peritoneum, such as appendicitis 
in the early stages, may cause a slight increase in blood-pressure, 
whereas renal colic, plumbic cramps, and tabetic crisis generally 
show a marked rise in tension. The onset of peritonitis is accom- 
panied by a distinct increase of pressure which gradually falls 
with increasing toxemia. The rise is due to local pressor, the fall 
to central depressor, impulses. 

The custom now instituted in all up-to-date clinics of having the 
anesthetist or his assistant chart the pulse rate and blood-pressure 
during the course of anesthesia, with the addition of occasional 
notes dictated by the operator, is most commendable. It is not 

1 Kato and Kotzenberg, Ueber d. Verhalten d. arteriellen Blutdruckes bei chirur- 
gischen Nierenerkrankungen u. Appendicitis, Beitr. z. klin. Chir., 190S, lviii, 404. 



MENSTRUATION 



395 



only a signal assistance to the surgeon at the time of the operation, 
but it also leads to a more careful analysis of the effects of anesthesia 
and trauma, and furnishes permanent records for statistical study. 




Fig. 97. — Chart from a case of gastromesenteric ileus, together with pyloric 
stenosis due to a healed ulcer, requiring a pyloroplasty in addition to resection of the 
right half of the colon. The operation lasted three hours and twenty minutes. No 
ether was used. A marked fall of pressure occurred while closing the peritoneum. 
This was remedied by temporarily placing the patient in the Trendelenburg position. 
Sudden cyanosis with a second fall of pressure occurred while the abdominal wound 
was being closed. The nitrous oxid was stopped and the operation finished under 
local anesthesia. Salt solution, strophanthin, and the inverted posture again restored 
the patient to a satisfactory condition. (After Bloodgood.) 



Menstruation. — Blood-pressure frequently rises for a day or 
two preceding the onset of menstruation. There is a fall of blood- 
pressure during the period which occurs independently of the loss 
of blood, and which has been attributed to a slowing of the pulse 
and to psychic factors. 1 It is lowest on the second day of the flow 

1 Wiessner, M., Ueber das Verhalten des Blutdruckes wahrend der Menstruation, 
etc., Leipsic, 1904. 



396 BLOOD-PRESSURE IN SURGERY AND OBSTETRICS 

and is not much affected by the occurrence of pain at this time. 1 
Large doses of atropin (0.00075 gm. hypodermically) have sometimes 
been successfully used in the treatment of dysmenorrhea of the 
spasmodic type associated with cramp-like pain a day or two 
before the onset of flow, especially in vagotonic cases. Much stress 
has been laid by Stolper upon the importance of blood-pressure 
estimations in the proper selection of cases. He states that women 
with a normal or slightly increased pressure during the inter- 
menstrual interval react most promptly to atropin, whereas those 
with a marked increase in blood-pressure show less response. 
Bogdanovics 2 and others have reported a premenstrual rise of blood- 
pressure in normal women, followed by a gradual decline after the 
onset of flow. Based upon pulse rate, blood-pressure, temperature, 
and muscular strength tests, the statement has been made that a 
cyclic rhythm occurs in normal women which renders them subject 
to periodic intervals of inefficiency. 3 The recent studies of King 4 
indicate that this tendency has been overemphasized and in so 
far as observations are concerned, made upon the systolic, diastolic 
and pulse pressures of eleven women, such irregular results were 
obtained that they do not support the wave theory. 

The Menopause. — Circulatory abnormalities are of frequent 
occurrence during the menopause. Among these "flashes of heat," 
formication, numbness, vertigo, cardiac palpitation, dyspnea on 
exertion, etc., may be encountered. A rise of arterial pressure is 
not uncommon after the cessation of menstruation. Whether it is 
merely a symptom or, as Potter 5 suggests, the cause of the symptoms, 
is uncertain. If pressure changes are marked and prolonged the 
possibility of renal disease must be borne in mind. 

Ovarian extirpation clinically often produces evidences of increased 
irritability of the sympathetic nervous system. This has been 
substantiated experimentally, since this operation in bitches results 
in from six to eight weeks in a markedly increased vasomotor 
reaction after one injection of nicotin. The reaction to epinephrin, 
however, is not increased. 6 

1 Tenji, T., Ueber d. Verhalten des Blutdruekes zw. d. Menstruellen u. nicht 
Menstruellen Ztschr., Arch. f. Gynak., 1909, lxxxix, 517. 

2 Zentralbl. f. Gynak., 1910, xxxiv, 994. 

3 Jacobi, The Question of Rest for Women during Menstruation, Boylston Prize 
Essay, 1876. 

4 Concerning the Periodic Cardiovascular and Temperature Variations in Women, 
Am. Jour. Physiol., 1914, xxxiv, 203. 

6 Blood-pressure at the Climacteric, British Med. Jour., December 2, 1911, p. 1472. 
6 Hoskins and Wheelon, Ovarian Extirpation and Vasomotor Irritability, Am. 
Jour. Physiol., 1914, xxxv, 119. 



PREGNANCY 397 

Extirpation of the testes is followed by a fall of blood-pressure, 
and the reaction to nicotin is constantly lowered. It would seem, 
therefore, that normally functionating testes bear a relationship 
to irritability of the sympathetic. 1 

Pregnancy. — Blood-pressure in a normal pregnancy rarely 
exceeds 120 mm. Hg., and readings of 140 mm. or more should be 
regarded with suspicion and carefully watched for eclamptic mani- 
festations. Even in the later months of gestation the average 
pressure ranges between 115 and 120 mm. 

What was previously described as the normal cardiac hyper- 
trophy in pregnancy is really only a change in the lateral percussion 
area, due to the more transverse position of the heart which the 
upward pressure upon the diaphragm entails (Stengel and Stanton) . 
This transverse position tends to cause a kinking of the large 
vessels, which adds to the work expended by the heart, and in the 
case of a diseased myocardium this factor may become important. 
It also explains the occurrence of accidental pulmonary murmurs. 
In normal women under thirty years of age, according to J. C. Hirst, 
the systolic pressure during the first eight months of pregnancy 
will average 118. In the last month it averages about 124. A 
slight fall may follow the subsidence of the uterus. 

In patients between thirty and forty years of age the pressure 
ranges between 126 and 128 mm. 

The normal relations between systolic and diastolic pressure 
should maintain. Cases showing a pulse pressure of or over 50 mm. 
should be watched and are often benefited by digitalis. 2 

The normal blood-pressure during the second stage of labor, if 
taken between uterine contractions, ranges between 130 and 150 
mm. After delivery normal values are reestablished. This fall 
is due to fatigue, cessation of excitement, and pain, as well as to 
vascular relaxation in the splanchnic domain. During the pains 
pressure estimations for obvious reasons cannot be made, but 
doubtless the pain as well as the abdominal compression cause 
much higher blood-pressure. Rupture of the membranes usually 
produces a marked but temporary fall in pressure. The birth of 
the child is again followed for a time by a fall of from 60 to 90 
mm. 3 These changes in blood-pressure are due to the sudden 

1 Wheelon, H., Influence of Testes on Blood-pressure, Am. Jour. Physiol., 1914, 
xxxv. 

2 Hirst, John C, Blood-pressure in Pregnancy, Penn. Med. Jour., May, 1915, p. 615. 

3 Heynemann, Th., Herz u. Zwerchfellstand wiihrund Schwangerschaft, Ztschr. f. 
Geburtsh. u. Gynak., 1913, Ixxiv, 854. 



398 BLOOD-PRESSURE IN SURGERY AND OBSTETRICS 

diminution of intra-abdominal tension, to which it takes some time 
for the vasomotor system to accommodate itself. Large hemor- 
rhages tend to delay the return of pressure to the normal. A rising 
pressure during the latter pari of pregnancy is the most constant 
symptom of gestational toxemia and is a frequent precursor of eclampsia 
(Hirst). 1 It is very important to know what the woman's usual 
pressure has been, otherwise the existence of a moderately high 
pressure may be over- or undervalued. The hypertension increases 
with the severity of the attack. Many of Edgar's cases showed 
pressures of 200 mm. or more. "A fall of blood-pressure with 
amelioration of the other symptoms is the most favorable prognostic 
sign, but with aggravation of other symptoms indicates impending 
death." Intermissions with lowered pressure are favorable omens. 
The other symptoms are generally an increased pulse rate, epi- 
gastric pain, headache, visual disturbances, edema, albuminuria. 
Cases with renal disease rarely pass through the period of gestation 
without some manifestations of toxemia. The absence of increased 
blood-pressure does not always exclude the possibility of eclampsia ; 
the presence of high pressure between convulsions does exclude 
epilepsy (Chirie). 

In the early stages of toxemia, gastro-intestinal symptoms may 
be marked before blood-pressure changes are obvious, and fatal 
convulsions may not be attended by a pressure over 160 mm. 
Hirst has reported a reading of 320 mm. in eclampsia and 192 mm. 
in a case of toxemia without eclampsia. He has seen recovery in 
two cases with pressures of 420 and 400 mm. respectively, showing 
that the danger of death is not necessarily proportionate to the 
height of pressure. The average eclampsia pressure ranges between 
190 and 200 mm. 

The administration of ergot does not appear to raise blood- 
pressure in the toxemia of pregnancy (see page 332), but the 
employment of pituitrin may cause a very marked rise (Hirst) . 

Summary. — During pregnancy a pressure of 125 mm. is normal; 
a pressure between 125 and 150 is to be regarded with suspicion; 
while a pressure of over 150 if accompanied by other toxemic 
symptoms calls for prompt and energetic treatment; often the 
induction of premature labor (J. C. Hirst). 

The Treatment of Eclampsia. — Some obstetricians of wide 
experience recommend the use of veratrum viride in the treatment 

1 The Importance of Blood-pressure in the Toxemia of the Latter Half of Preg- 
nancy, New York Med. Jour., 1910, xci, 1204. 



TREATMENT OF ECLAMPSIA 399 

of eclampsia. Hirst states that "the most successful remedial 
measures are those which reduce blood-pressure most quickly and 
most effectually, such as puncture of the membranes, sweating, 
purgation, venesection, veratrum viride, and nitroglycerin," while 
Edgar writes: "I prefer ether, veratrum viride, glonoin, and chloral 
in the order named." Now clinical results are of primary impor- 
tance, but in view of some definitely established facts it would 
appear that they are open to revision. We have seen under the 
discussion of nephritis that hypertension often appears to be 
Nature's defense against anuria and coma, and the most experi- 
enced clinicians no longer attempt to reduce blood-pressure by 
direct means except in cases of an emergency. Is eclampsia such 
an emergency? The reduction of pressure allays the convulsions, 
but is this due to the fact that the patient is too depressed to 
respond to stimuli? It has been established that collapse and 
shock are associated with and are in part the result of low blood- 
pressure. By administering cardiovascular depressants are we 
not reducing our eclamptic patient to a condition of collapse? It 
has been shown that rapid emptying of the uterus in eclampsia 
frequently produces a fall of blood-pressure amounting to 100 mm. 
Hg., while a full dose of veratrum viride of itself may cause a 
depression of 145 mm. 1 It is unpleasant to contemplate the degree 
of blood-pressure fall which a combination of these two procedures 
might entail. Even if the eclamptic rise of pressure is not of a 
protective nature, and even if it should appear desirable to lower 
pressure by medicinal means, it would seem far preferable to do 
so by the administration of the nitrites — drugs which do not also 
depress the heart and the medullary centres. Chloroform is 
undesirable not only because of its effect upon the heart, but also 
on account of its tendency to produce necrosis of the hepatic cells. 
Eclampsia is more than a vascular crisis, and while much higher 
blood-pressure favors and doubtless precipitates visceral hemor- 
rhages, such a rise of tension is only a symptom and not the basis 
of gestational intoxication. So far as the writer is aware, blood- 
pressure readings yield no clue as to the relative indication for 
immediate Cesarean section or conservative treatment. 

Hyperemesis gravidarum is usually associated with hypotension, 
perhaps as a result of impoverished nutrition, 2 and indicating that 
the toxin is different from that causing eclampsia. 

1 Bailey, A. C, Shock in Eclampsia, Am. Jour. Obstr., 1911, Ixiv, No. 2. 

2 Wallich, V., L'hypertension gravidique, Ann. d. Gynec. et d'Obstr., 1912, xxxix, 
G53. 



400 BLOOD-PRESSURE IN SURGERY AND OBSTETRICS 

In extra-uterine pregnancy the occurrence of anemia with a fall 
of pressure is the most important indication of internal hemorrhage 
(Horner). 

Attention has been called to the fact that shock associated with 
and probably due to low blood-pressure may, even in the absence 
of large hemorrhages, lead to sudden death during childbirth. 
Women with pressures not exceeding 90 mm. may pass through 
labor normally, but such low readings, especially if associated 
with anemia, always indicate special care and the institution of 
such measures as tend to prevent shock. 1 Poorly developed, 
neurasthenic women or women with contracted pelves often have 
low pressures. 




Fig. 98. — McKeson's sphygmomanometer for use during operations (Gwathmey.) 



Blood-pressure Observations during Anesthesia. — With the 
intention of rendering blood-pressure readings much easier during 
anesthesia, Nicholson has fitted his new pocket sphygmoman- 
ometer with a Fedde indicator, in which a pith-ball plays up and 
down as long as pulsations of pressure are transmitted to it. This 
is attached to the left-hand side of the box and connected up with 
the manometer and two cuffs, one above and one below the elbow 
or knee-joints. 



1 Lynch, F. W. 
1913, xvii, 472. 



Blood-pressure during Pregnancy, Surg.. Gynec. and Obstr.. 



BLOOD-PRESSURE OBSERVATIONS DURING ANESTHESIA 401 

An air pressure of about 80 mm. may be maintained in the lower 
cuff throughout the operation, and the character, volume, and rate 
of the pulse noted continuously. The anesthetizer inflates the upper 
cuff with one hand whenever he desires to know the systolic pressure, 
simply noting the height of the mercury column when the pith- 
ball ceases oscillating. He then releases the air pressure in the 
upper cuff and continues the anesthesia. In perineal operations 
the cuffs are placed on the arm and forearm instead of the thigh 
and leg. 



20 



CHAPTER XVIII, 



OPHTHALMOLOGY. 



Since the ophthalmoscope is the only instrument which renders 
the naked arteries and veins visible during life it is not surprising 
that important data regarding blood-pressure or stasis, or vascular 
degeneration should be forthcoming from this source. The char- 
acteristic retinal lesions due to arteriosclerosis and arterial hyper- 
tension are not infrequently discovered by the ophthalmologist 
before other symptoms cause the patient to consult his physician. 
Ophthalmoscopic examinations are of value to the student of 
blood-pressure no less than are sphygmomanometric estimations 
to the ophthalmologist. 




Fig. 99. — Rubino's modification of the Bloch-Verdin Sphygmometer. 

Blood-pressure in the Retinal Arteries.— The maximal pressure 
in healthy retinal arteries ranges between 80 and 112 mm. Hg. 
according to Rubino, who has modified the Bloch-Verdin apparatus 
for its measurement. The determination is based upon the principle 
that a certain pressure exerted upon the eyeball will arrest the 
circulation, this being indicated by the temporary loss of sight in 
the eye in question (Fig. 100). 

The Relation of Blood-pressure to Ocular Tension.— For practical 
purposes the eye may be regarded as an inelastic capsule, having a 
tension greater than the atmosphere, which varies as the intra- 
ocular contents are increased or decreased. Such changes are 
brought about mainly by alterations in the blood-supply, the 



RELATION OF BLOOD-PRESSURE TO OCULAR TENSION 403 

vitreous or the aqueous. "The circulatory conditions in the eye 
resemble those in the intracranial cavity, with the exception that 
the intra-ocular is much higher than the intracranial pressure, 
and is therefore not affected by changes in the general venous 
pressure" (Hill and Flack 1 ). Intra-ocular tension generally varies 




Fig. 100. — The Rubino instrument in use. 




Fig. 101. — The Bajardi instrument for estimating retinal arterial pressure. 2 



with arterial pressure, but peripheral vasodilatation which lowers 
systemic pressure tends to increase intra-ocular pressure. Normally 

1 I. The Relation between Capillary Pressure and Secretion. II. The Secretion 
of Aqueous and the Intra-ocular Pressure, Proc. Roy. Soc., Series B, August 12, 
1912, xxxv. 

2 La pressione del sangue nell' arteria retinica e suoi rapporti con la pressione nel 
cercolo del Willis, Riforma Med., 1911, xxvii, 1345. 



404 OPHTHALMOLOGY 

any change of tension is compensated by a reciprocal lymphatic 
flow. Excluding external causes (eyelids, ocular muscles, tumors of 
the eyeball or orbit), changes in tension mean loss of secretory 
compensation, which may come about "either by mechanically 
blocking the normal excretory channels or by so altering the normal 
ciliary secretion as to interfere with its ready interchange" — the 
"secretion" of the ciliary body is not truly a secretion in the physi- 
ologic sense of the term, but an osmotic process, the passage of 
fluid through a dialyzing membrane. There are no lymphatics 
in the eye, and the iris and vitreous have no secretory function." 
According to Starling and Henderson the difference between arterial 
and intra-ocular tension averages 84 mm., and it is upon these 
pressure differences that the rate of secretion depends. The specific 
gravity of the secretion varies directly with blood-pressure and 
inversely with ocular tension. "Permanently increased tension 
is not due to high blood-pressure directly, but may coexist with 
it only in the absence of adequate compensation" (Ibershoff), 
(see page 43) . 

The foregoing statements are generally accepted. In opposition 
to them Henderson believes that intra-ocular and intracranial 
tension run closely parallel. The latter depends much more upon 
the general venous than upon the general arterial pressure. It 
varies directly and absolutely with the pressure in the vena cava, 
which makes itself felt at once by backward pressure on the cerebral 
venous capillaries. A rise of arterial pressure only produces a 
proportional rise in the intracranial pressure, because between 
the aorta and the cerebral veins lies the unknown and varying 
resistance of the arterioles. 

Based upon experimental evidence, Henderson believes that 
what has just been stated regarding intracranial tension applies 
to intra-ocular pressure, except that response in the latter is less 
prompt owing to the ramifications of the ocular veins. Therefore 
"the intra-ocular pressure mvst be the same as the infra-ocular venous 
-pressure." Since the corneoscleral envelope is an unyielding case 
with a fixed cubic capacity, analogous in every respect to the bony 
cranium, the intra-ocular pressure is not a question of volume of 
the intra-ocular contents but purely a question of pressure of a 
fixed volume, which is governed in turn by the intra-ocular and 
general venous pressure. The intra-ocular pressure therefore 
respresents "the pressure which remains in the eyeball after the 
force of the heart has been expended in driving the blood through 



RE L ATI OX OF BLOOD-PRESSURE TO OCULAR TENSION 405 

the intra-ocular arterioles. On account of the elastic nature of the 
circulatory system of tuhes a rise of arterial pressure can only 
produce an increase in intra-ocular pressure in proportion as the 
resistance in the arterioles is overcome and intravenous pressure 
raised." 1 

The Estimation of Intra-ocular Tension. — The old method of 
gauging ocular tension, which for practical purposes may be con- 
sidered synonymous with intra-ocular pressure, by means of the 
fingers, is for obvious reasons falling into disuse when anything 




Fig. 102. — The Schiotz tonometer. 



like accurate measurement is desired. The tactus eruditus cannot 
compete with instrumental precision. Several instruments are 
now available for the purpose. Among these the Schiotz tonometer 
has received wide-spread commendation (see Fig. 102). 

Intra-ocular tension is rated with this instrument by measuring 
the depth of the depression produced in the anesthetized cornea 
by the weight of the shaft of the tonometer; the higher the tension, 
the less the depression. The data obtained are, however, based 

1 Henderson, T., Glaucoma, E. Arnold, London, 1910. 



406 OPHTHALMOLOGY 

upon (1) the elasticity of the sclera and cornea, (2) the intra-ocular 
tension, and (3) the condition of the ocular drainage system. 1 
Normal readings should not exceed 26 mm. Hg. ; the normal pressure 
is about 20 mm. 

As with other ocular tonometers, considerable practice is required 
before accurate readings can be obtained. Even with careful 
application considerable discomfort to the patient is entailed. No 
pressure should be made upon the eyeball except that exerted by 
the weights. 

The Stephenson tonometer is applied over the closed upper lid. 
It is furnished with a handle for holding it in position on the patient's 
face and with a milled head for adjustment to varying depths. 
The end of the inner tube, which consists of a concave cup, contains 
a spiral spring actuated by a jointed lever. The instrument is 
adjusted to zero, the lever makes pressure upon the eye, and the 
moment at which indentation occurs is shown on the indicator. 
Since the tension of the orbicularis palpebrarum and the recession 
of the eyeball into the orbit are fairly constant in a given individual, 
temporal variations of pressure can be estimated. The technique 
with this instrument is easily acquired. No anesthetic is necessary 
and readings may be made in about one minute. Just what pro- 
portion of the pressure obtained is true intra-ocular tension and 
how much is pressure of the retrobulbar tissues is as yet not posi- 
tively determined. 2 

Ocular Lesions due to Increased Arterial Pressure. — This 
subject cannot of course be discussed here in extenso. "In the 
later stages of intra-ocular vascular disease, hemorrhages fre- 
quently appear. If centrally placed, their very position interferes 
with vision, or they may invade the vitreous, may result in pro- 
liferating retinitis, may cause glaucoma, and, if extensive, detach- 
ment of the retina. Closely allied to vascular changes are also 
lenticular cataract, some varieties of optic atrophy, and some cases 
of retrobulbar neuritis" (de Schweinitz). According to William 
F. Norris, retinitis in some form occurs in not less than 25 per cent, 
of all cases of Bright's disease seen in general hospitals. 

In a study of 104 cases of ocular disease, Peter 3 found blood- 
pressure as follows: 

1 Schonberg, M. J., Experimental Study of Intra-ocular Pressure and Ocular 
Drainage, Jour. Am. Med. Assn., 1913, lxi, 1098. 

2 Reber, W., A Clinical Study of Ocular Tonometers, Pennsylvania Med. Jour., 
1913, xvii, 281. 

3 Peter, L. C, Arterial Hypertension and its Relation to Morbid Changes in the 
Eye, Pennsylvania Med. Jour., 1911, xiv, 411. 



OCULAR LESIONS AND ARTERIAL PRESSURE 407 

9 syphilitic neuroretinitis, average systolic blood-p essure .... 132 mm. 

3 chronic parenchymatous nephritis, average systolic blood-pressure . 132 " 

20 retinitis, average systolic blood-pressure 165 " 

59 neuroretinitis, average systolic blood-pressure . . . ' . . . . 185 " 

3 albuminuric retinitis, average systolic blood-pressure 190 " 

6 hemorrhagic retinitis, average systolic blood-pressure 205 " 

3 papillitis, average systolic blood-pressure 225 " 

Lenticular Cataract. — What has already been said regarding the 
effect of arterial hypertension in altering the osmotic balance of 
the ocular fluids may in a measure apply to lenticular cataract, 
if we assume that clouding of the lens is due to an abnormal dialysis 
between the anterior and the posterior chambers of this structure. 

Glaucoma. — The general consensus of opinion appears to be that 
arterial hypertension bears only an indirect relation to glaucoma. 
This condition, which is predisposed to by a large lens and a small 
cornea, may be precipitated by a congestion or hemorrhage in the 
ciliary region which interferes with the compensating mechanism. 
"In the former the heightened blood-pressure causes increased 
secretion which in the presence of altered arterial walls is of a 
higher specific gravity than normal, so that the already impaired 
drainage is further embarrassed and compensation fails. In the 
case of hemorrhage, the lymph mixed with blood clogs the outflow 
channels and failure of excretion follows" (Ibershoff). If the 
foregoing facts are accepted, operative measures should not be 
attempted without first lowering arterial pressure, since the opening 
of the anterior chamber or of the sclera would be followed by 
"the rapid reformation of ocular fluids of a much higher specific 
gravity and osmotic coefficient." The danger of expulsive hemor- 
rhage would also be diminished if systemic pressure were lowered. 
Craggs and Taylor, from several hundred comparisons, were unable 
to establish any relations between glaucoma and increased arterial 
tension. 1 McRae's 2 studues of 20 cases lead him to draw similar 
conclusions. 

Lohlein, 3 who studied some twenty cases of glaucoma by com- 
paring the general blood-pressure, the intra-ocular pressure, and 
the adrenalin content of the blood, was unable to corroborate 
Kleczkowski's statement that a definite relationship existed. It is 
generally conceded, however, that no study of either acute or 

1 Craggs, H. C, and Taylor, C. G., A Research into the Relation between Systemic 
Blood-pressure and Raised Intra-ocular Tension, Ophthalmoscope, 1913, xi, 350. 

2 Ophthalmoscope, April, 1915, p. 168. 

3 Ueber Blutuntersuchungen bei Glaucomkranken, Graefe's Arch. f. Ophthal., 
lxxxiii, 547. 



408 OPHTHALMOLOGY 

chronic glaucoma is complete without a record of the systemic 
arterial tension. 

The belief that primary glaucoma is the product of retention 
of intra-ocular volume has been widely accepted. In opposition 
to this hypothesis, Thomas Henderson offers a different explanation. 
Every case of primary glaucoma depends upon (1) a constant 
predisposing sclerotic factor, and (2) on the variable vascular factor 
which is directly due to the general circulatory pressure. Since 
neither the eye nor the brain possesses any protective circulatory 
mechanism, "a rise in the vena cava pressure produces, millimeter 
for millimeter, a corresponding and equal rise in intra-ocular and 
intracranial pressures, while increase of pressure in the aorta causes 
a rise of pressure in the eye and brain whose exact amount depends 
on the varying resistance of the arterioles. Glaucoma therefore 
may be caused by a rise of arterial pressure, but is specially to be 
feared when there is a rise of the general venous pressure. This 
in an eye with a sclerotic cribriform ligament, and therefore a 
diminished access of aqueous to the veins, precipitates the attack. 1 

Retinal Hemorrhages. — Retinal hemorrhages often show a more 
or less direct relation to increase of vascular tension, and ocular 
changes are most commonly noted in severe cases of nephritis at 
the time at which the pressure is highest. Thus hemorrhages into 
the retina are often precipitated by, and directly attributable to 
conditions which suddenly raise the intracranial arterial pressure, 
such as lifting, stooping, straining, etc. 

The presence of retinal hemorrhages in a case of chronic arterial 
hypertension point almost indubitably to a severe nephritis. 
Retinal changes in nephritis have been reported as follows: Wagner 
in 6 per cent, of 157 cases, Frerichs in 15 per cent, of 41 cases. 
Lecorche in 22 per cent, of 286 cases, Eales in 28 per cent, of 100 
cases of chronic kidney disease, Miles Miley in 31 per cent, of 
104 cases of acute and chronic kidney disease, Galezowski in 31 
per cent, of 154 cases. 

The duration of life after the first retinal changes were noted: Bull 
reported 103 cases: 86 of the patients died, 57 within the first 
year, 18 in the second year, 6 in the third year, 4 in the fourth 
year, and 1 in the sixth year of observation, making S7 per cent. 
in the first two years. Miles Miley, in 164 patients with acute 
or chronic kidney disease, found 105 with healthy eyes and 51 with 

1 Henderson, Thomas, Glaucoma, London. 1910. 



PULSATION OF THE RETINAL VESSELS 4(1!) 

retinitis albuminurica (the other 8 had affections of the eyes which 
are not pertinent to onr subject); 27 per cent, of the former and 
53 per cent, of the latter died. The mortality shown among those 
Inning retinitis albuminurica was twice as great as among patients 
with healthy eyes. Most of the patients lived about twelve months 
after the first indications of retinal changes, two lived nearly 
fourteen months, and one about eighteen months. In those cases 
in which the onset of the retinal disturbance could be definitely 
established the average duration of life did not exceed six months. 1 
(see page 292). 

The existence of high systemic blood-pressure is of ophthalmologic 
interest in relation to postoperative hemorrhage after cataract 
extraction and in spontaneous subconjunctival hemorrhages, although 
the latter may for other reasons occur with normal or even low 
arterial tension. The higher the arterial tension, the less favorable 
is the case from an operative stand-point. In such cases vasodila- 
tors may be administered to reduce pressure during the operation. 
Morphin is also useful, since it helps to prevent the emotional 
disturbance with which a cataract extraction is of necessity asso- 
ciated, and which has such a potent pressor effect. 2 

Spasm of the retinal arteries of variable duration and of not 
infrequent recurrence is now a well-established ophthalmologic 
entity. The vascular spasm has been observed in its incipience 
and disappearance by means of the ophthalmoscope. There seems 
to be a growing conviction that a number of the cases which were 
previously attributed to embolism were really instances of spastic 
arterial contraction. The literature on the subject has been sum- 
marized by Zentmayer, 3 who also reported a case in which he 
repeatedly observed a spasm of the central retinal artery. The 
condition is generally associated with arteriosclerosis and hyper- 
tension, and causes temporary blindness, usually of the hemianopic 
type (Peter) " (see Vascular Crises, page 25G). 

Pulsation of the Retinal Vessels. — Blood-pressure in the oph- 
thalmic artery of animals is only a few millimeters Hg. below that 
of the carotid. While this relation may not hold good for man, 

1 Quoted by Posey, W. C, The Significance of Ocular Findings in Estimating 
Longevity, Jour. Am. Med. Assn., 1913, lx, 1867. 

2 Reber found a rise of pressure of 30 mm. occasioned by the psychic stimulation 
incident to preparation for a cataract extraction. 

3 Pome Unusual Ocular Manifestations of Arteriosclerosis, Jour. Am. Med. Assn., 
1906. 

1 Arterial Hypertension and its Relation to Morbid Changes in the Eye, Pennsyl- 
vania Med. Jour., 1911, xiv. 111. 



410 OPHTHALMOLOGY 

arterial pressure is well above the intra-ocular tension. Under 
normal conditions the vascular pulsation cannot be ophthalmo- 
scopically demonstrated, probably because the pulsatile movement 
is damped by the intra-ocular tension, and because it is spread 
over the large area of the eyeball. 

Under pathologic conditions, aortic insufficiency, aneurysm, 
exophthalmic goitre, etc., arterial pulsation can sometimes be 
seen either as (1) "a true pulse wave, accompanied by locomotion 
of the vessels, and (2) an intermittent flow of blood or pressure 
pulse. In the latter instance, the arteries fill with blood only with 
the heart beats, being empty between them; and pulsation is only 
visible upon the disk. This type of pulsation is a pure pressure 
phenomenon, and is caused by any considerable increase of intra- 
ocular tension with normal or lowered blood-pressure, as in glaucoma, 
or by any considerable diminution of blood-pressure with normal 
intra-ocular tension, as in syncope, orbital tumors, etc. The true 
arterial pulse occurs in cases of aortic regurgitation (Quincke) or 
aneurysm, in Graves's disease, etc.; it is not confined to the optic 
disk. It is equally a pressure phenomenon, but the differences of 
pressure are smaller." 

"Capillary pulsation is seen only in aortic regurgitation as a 
systolic reddening and diastolic paling of the disk." Venous 
pulsation occurs in three forms: (1) the normal negative venous 
pulse; (2) the positive venous pulse (tricuspid insufficiency), and 
(3) the transmitted centripetal venous pulse (an exaggerated form 
of the normal type due to venous congestion). 1 

A careful ophthalmoscopic examination, in conjunction with 
blood-pressure studies, is therefore often of the greatest value. 
It should be made with a dilated pupil, as minor degrees of vascular 
changes are easily overlooked, but strong mydriatics, such as 
atropin, should not be used on account of the danger of precipita- 
ting an attack of glaucoma. De Schweinitz recommends euph- 
thalmin (3 drops of a 5 to 10 per cent, solution) to be followed after 
the examination by the instillation of a few drops of a solution 
of pilocarpin, gr. j to the ounce. 

Visual Accommodation. — Systemic blood-pressure also bears a 
relation to visual accommodation which is apt to be better late in 
the day when pressure is at its highest. Hypotensive individuals 
often have less accommodative power. The onset of presbyopia is 

1 Parsons, Pathology of the Eye, 190S, iv, 1254. 



THE EYE-GROUNDS IN ARTERIAL HYPERTENSION 411 

often concomitant with the beginning of arterial hypertension 
(de Schweinitz). Attention has also been called by this eminent 
author to the fact that certain forms of asthenopia, especially those 
occurring in women in the late forties, owe their origin to angio- 
sclerosis, and while rebellious to the usual methods of treatment, 
yield to dietetic and therapeutic measures which tend to lower 
arterial tension. 

A large percentage of the early cases of increased blood-pressure 
are overlooked unless the sphygmomanometer is employed, and 
likewise many cases of incipient arteriosclerosis will not be detected 
if the ophthalmoscope is not called into requisition. This applies 
especially to those cases in which the arterial involvement is chiefly 
cerebral. 

In 90 cases of general arteriosclerosis Rahlmann 1 found macro- 
scopic lesions of the vessels of the retina in practically all. Well- 
marked changes occurred in about 20 per cent. 

The Eye-grounds in Arterial Hypertension. — "The eye-ground 
lesions of persistent high arterial tension, when this is a symptom 
of arteriosclerosis, may conveniently be divided into those which 
are suggestive and those which are pathognomonic. The suggestive 
signs include uneven caliber and undue tortuosity of the retinal 
arteries, . increased distinctness of the central light streak, an 
unusually light color of the breadth of the arten-, and alterations 
in the course and caliber of the veins." 

The pathognomonic signs include changes in the size and breadth 
of the retinal arteries of such character that a beaded appearance 
is produced; distinct loss of translucency; decided lesions in the 
arterial walls, consisting of white stripes in the form of perivasculitis; 
alternate contractions and dilatations of the veins, and particularly 
— and this is the most important of the signs — indentation of the 
veins by the stiffened arteries in the same manner as a solid rod 
would indent a rubber tube when lying across it. Sometimes the 
vein is simply flattened slightly at the point of crossing, or merely 
pushed aside, or its caliber is contracted so that beyond the point 
of crossing there is an ampulliform dilatation. In addition to these 
clear signs there may be changes in the venous walls so that they 
are bordered with white stripes. The veins may be exceedingly 
tortuous and contain varicosities. Finally, there are edema of the 
retina in the form of gray opacity around the disk or following 

1 Quoted by de Schweinitz, Intraocular Angiosclerosis and its Prognostic and 
Diagnostic Significance, Internal. Clinics, series 17, i, 177. 



412 OPHTHALMOLOGY 

the course of the vessels; hemorrhages manifesting themselves as 
linear extravasations or roundish infiltrations, or sometimes assum- 
ing a drop-like form" (de Schweinitz) - 1 

The Ocular Reflex. (Aschner). — If sufficient pressure is exerted 
upon the eyeball beneath the supra-orbital ridge, the eye being 
turned downward so as to avoid pressure upon the cornea, a reflex 
lowering of the pulse will normally occur. The reflex inhibition, 
as has been experimentally demonstrated, travels over the fifth 
to the tenth nerve. The reflex has been found exaggerated in 
epilepsy, and in exophthalmic goitre. It is not abolished by ether 
anesthesia. It is increased by the administration of pilocarpin 
and diminished by atropin. Considerable pressure is required to 
bring about the reflex, and this in turn entails a good deal of pain 
to the patient and perhaps danger to some eyes. It is not a 
procedure which can be readily or frequently applied, and should 
therefore be reserved for the study of exceptional cases. The 
pressure above mentioned will sometimes slow the pulse when 
direct pressure over the vagus in the neck fails to do so. It is inter- 
esting to remember that Robinson and Draper have shown that the 
right vagus inhibits the heart more than does the left, and similarly 
pressure over the right eye seems to especially exert its effect upon 
the sinus region of the heart, whereas pressure over the left eye seems 
to exert more influence upon the conductive system (Levine). 

The reflex is said to be positive when a slowing of the pulse 
occurs. Normally when it occurs the reflex is positive. The 
absence of pulse retardation or an actual increase in rate occurs in 
sympathicotonics. In vagotonics, on the other hand, marked slow- 
ing of the pulse occurs. Indeed, in them pressure maintenance for 
ten to twelve seconds may cause syncope from complete temporary 
asystole. These symptoms are due to an abnormally low nervous 
threshold in the vagus system, since they disappear under atropin. 2 
The claim that the reflex is of diagnostic value in differentiating 
cardiac weakness due to myocardial lesions from those due to nervous 
disturbances has not been substantiated. It may be of some value 
in differentiating between postfebrile bradycardia and auriculo- 
ventricular heart block. 3 This reflex is generally absent in tabes 
dorsalis. 

1 Loc. cit. 

2 Neugebauer, H., Beitr. z. Klinik d. Vagotonic, Wien. klin. Wchnschr., 1914, 
xxvii, 1023. 

3 Gunson, E. B., The Oculocardiac Reflex, British Jour. Child. Dis., 1915, xii, 
No. 136, p. 97. 



INDEX. 



Abdominal aorta, paroxysmal dilata- 
tion of, 259 
Acromegaly, blood-pressure in, 352 
Addison's disease, blood-pressure in, 

349 
Adiposity, blood-pressure in, 269, 354 
Adrenal glands, physiology of, 33, 280, 
330 
in nephritis, 279 
insufficiency, acute, 381 
white line in, 263 
Age, blood-pressure and, 53 
Air, cold, effect on blood-pressure, 205 
Albuminuria, blood-pressure and, 287 

orthostatic, 191 
Alcohol, blood-pressure effects of, 324 
Alcoholism, blood-pressure in, 231 
Alkalies, blood-pressure and, 325 
Altitudes, blood-pressure and, 50, 357 
Ammonium, blood-pressure effect of, 

325 
Amyloid renal disease, 274 
Anaphylaxis, 210 
Anemia, blood-pressure in, 355 
Aneroid sphygmomanometer, 108 
Anesthesia, blood-pressure during, 400 
chilling during blood-pressure and, 
384 
Anesthetics, blood-pressure and, 388 
Aneurysm, aortic, blood-pressure in, 

239 
Angina abdominalis as vascular crisis, 
259 
pectoris as vascular crisis, 257 
Angioneuroses, blood-flow in, 262 
Angioneurotic edema, vascular crises 

and, 263 
Aorta, abdominal, paroxysmal dilata- 
tion of, 259 
Aortic aneurysm, blood-pressure in, 239 
insufficiency, blood-pressure in arm 
in, 236 
in leg in, 236 
Durozier's sign of, 238 
Traube's sign of, 238 
lesions, blood-pressure in, 235 
obstruction, blood-pressure in, 238 



Aortitis, syphilitic, blood-pressure in, 

213, 235, 288 
Apoplexy, 261, 295, 300, 373 

in vascular crises, 261 
Arhythmia, extrasystolic, blood-press- 
ure in, 242 
Arm, blood-pressure in, in aortic insuffi- 
ciency, 236 
estimation of blood-flow in, 167 
Arsenic poisoning, blood-pressure in, 

228 
Arterial blood-pressure, constitution- 
ally low, 185 
function, estimation of, 173 
hypertension, 299 
pressure, ocular lesions due to, 

406 
tonus, estimation of, 174 

Vries-Reilingh's method, 
174 
Arteries in arteriosclerosis, 252 

coronary, effect of epinephrin, 330 
effects of alterations of blood-press- 
ure on, 54 
functional tests of, 255 
physiology of, 28 
retinal, blood-pressure in, 402 
pulsation of, 409 
spasm of, 409 
in symptoms of arterial hyper- 
tension, 270 
Arteriocapillary index in blood-press- 
ure, 255 
Arterioles, effects of alterations of 
blood-pressure on, 55 
physiology of, 29 
Arteriosclerosis, arteries in, 252 

bilateral variations of pressure in, 

253 
blood-pressure in, 250 

in tobacco poisoning, 228 
ice reaction in, 255 
nitrite test of, 254 
stasis reaction in, 255 
vascular reactions in, 252 
Aspiration of pleura, blood-pressure 

effect of, 386 
Asthma, bronchial, blood-pressure in, 
249 



414 



INDEX 



Athletics, blood-pressure and, 46, 149, 
305, 365 

Atropin, blood-pressure effect of, 325 

Aural symptoms of arterial hyperten- 
sion, 270 

Auricular fibrillation, blood-pressure in, 
243 

Auto-intoxication, blood-pressure in, 
350 



B 



Bajardi's ocular sphygmomanometer, 

403 
Barach's formula of blood-pressure 

quotient, 161 
Barometric pressure, 358 
Bendick's sphygmomanometer, 82 
Berberin, blood-pressure effect of, 333 
Bichloride of mercury poisoning, 296 
Biliary colic and vascular crises, 260 
Bing's sphygmomanometer, 106 
Birth, blood-pressure at, 361 
Bishop's sphygmomanometer, 79 
Bladder drainage, effect on blood-press- 
ure, 388 
Bleeding. See Hemorrhage, phlebot- 
omy, 314, 355, 381. 
Blood and blood-pressure, 34 
Blood-flow in angioneuroses, 262 
blood-pressure and, 35 
estimation of, 163 
in arm, 167 

Bornstein's method, 170 
dynamic diagrams in, 179 
Fellner's method, 170 
Hewlett's method, 170 
Stewart's method, 163 
plethysmograph in, 166 
tachograph in, 171 
Van Zwaluwenburg's method, 

170 
von Kries's method, 171 
in fevers, 197 
renal function and, 281 
systolic output, estimation of, by 
venous pressure, 164 
Blood-pressure, absolute sphygmogram 
in, 156 
in acromegaly, 352 
in acute endocarditis, 234 

nephritis, 296 
in Addison's disease, 349 
in adiposity, 269, 354 
age and, 53 
albuminuria and, 287 
alcohol and, 324 
in alcoholism, 231 
alkalies and, 325 

alterations of, effects of, on arte- 
ries, 55 



Blood-pressure, alterations of, effects 
of, on arterioles, 55 
on capillary pressure, 55 
on heart, 54 
on kidneys, 56 
on organs of body, 54 
on pulmonary pressure, 

55 
on venous pressure, 55 

altitudes and, 50, 357 

ammonium and, 325 

in anemia, 355 

anesthetics and, 400 

in aortic aneurysm, 239 
lesions, 235 
obstruction, 238 

in arm, in aortic insufficiency, 236 

in arsenic poisoning, 228 

arterial, constitutionally low, 185 

arteriocapillary index in, 255 

in arteriosclerosis, 250 

in aspiration of pleura, 386 

athletics and, 46, 149, 305, 365 

atropin and, 325 

in auricular fibrillation, 243 

in auto-intoxication, 350 

bandaging of extremities and, 315 

and barometric pressure, 358 

berberin and, 333 

in bichloride of mercury poisoning, 
296 

at birth, 361 

blood in, 34 

blood-flow and, 35 

in bradycardia, 242 

bromides and, 330 

in bronchial asthma, 249 

in cachexia, 356 

caffein and, 326 

camphor and, 327 

capillary, estimation of, 175 

in carcinoma, 356 

cardiac cycle in, 25 

in cardiac disease, 233 

in cerebral hemorrhages, 372 

chemical regulation of, 33 

in Cheyne-Stokes respiration, 290 

in childhood, 53, 360 

chilling during anesthesia and, 3S4 

and climate, 359 

chloral and, 330 

after chlorin gas inhalation, 228 

chloroform and, 389 

in chlorosis, 356 

in cholera, 199 

cocain and, 390 

in collapse, 210 

counterirritation and, 319 

cuff, 59 

location of, 61 

in delirium tremens, 231 



I.XDEX 



41.3 



Blood-pressure in dementia precox, 371 

in diabetes, 347 

diastolic, 37, 130, 266 

diet and, 305 

digestion, effect of, 49 

digitalis and, 327 

in diphtheria, 199 

in diseases of heart, 233 
of myocardium, 241 
of nervous system, 369 

during anesthesia, 400 

and dysmenorrhea, 396 

in eclampsia, 398 

edema and, 241 

electricity and, 315 

in encephalopathy, 227 
treatment of, 228 

in epilepsy, 371 

epinephrin and, 330 

ergot and, 332 

erythrol tetranitrate and, 338 

estimation of, 58 

accuracy of, 130 

auscultatory, 66 

graphic method of, 83 

instrumental, 58 

oscillatory method of, 102 

palpatory, 62 

personal equation of examiner 

in, 127 
possible accidents in, 129 
precautions in, 125 
sources of, error in, 122 
subjective method of, 119 
technique of, 125 
value of, 130 
visual method of, 102 

ether and, 388 

ethyl chlorid and, 389 

exercise and, 46, 149, 305, 365 

in exogenous intoxications, 225 

in exophthalmic goitre, 352 

in extrasystolic arhythmia, 242 

in extra-uterine pregnancy, 399 

extremes, compatible with life, 131 

factors maintaining, 24 
regulating, 24 

feeding and, 49 

fluid intake and, 308 

fresh air and, 205 

in gastro-enteritis, 367 

glandular extracts and, 351 

in glaucoma, 407 

gonads, effect of, 399 

in gout, 348 

hormonal and, 334 

heart in, 24 

in hemiplegia, 374 

in hemorrhage, 355, 381 

in hemorrhages of brain, 372 

hemic viscosity and, 297 



Blood- pressure, hydrastinin and, 334 

hydrastis and, 333 
hydrotherapy and, 309 
in hydrothorax, 222 
in hyperemesis gravidarum, 399 
hyperglycemia and, 285, 347 
in infants, 360 
in infectious diseases, 196 
acute, 199 
chronic, 213 
treatment of, 209 
instruments, choice of, 132 

classification of, 133 

different types of, 133 

graphic registration, 87 
intra-abdominal, 41 

estimation of, 183 

Moritz's method, 183 

increased, 260 
intracranial, 42 
intra-ocular, 43 
intrapericardial, 41 
iodids and, 334 
in jaundice, 349 
kidneys and, 275, 286 
in lead poisoning, 225 
in leg, in aortic insufficiency, 236 
in lenticular cataract, 407 
life insurance and, 359 
in locomotor ataxia, 374 
in lumbar puncture, 391 
lymph flow and, 34 
mean, estimation of, 37 
in malaria, 201 

manipulations of pelvic viscera 
and, 386 

of thoracic viscera and, 386 
mannitol nitrate and, 338 
massage and, 318 
maximum, 22 

measurement of, method of, 19 
in meningitis, cerebrospinal, 202 

tuberculous, 202 
in menopause, 396 
in menstruation, 395 
in mental diseases, 370 
in mercurial poisoning, 296 
in metabolic diseases, 347 
minimum, 22 
mistletoe and, 336 
in mitral insufficiency, 239 

obstruction, 240 

stenosis, 241 
morphin and, 339 
in morphinism, 232 
muscular exertion in, 46, 149, 305, 

365 
in myxedema, 354 
Nauheim baths and, 309 
neosalvarsan, 342 
in nephritis, 272 



416 



INDEX 



Blood-pressure in neurasthenia, 369 
in neuroses, 369 
nitrites and, 336 
nitrogen retention and, 285 
nitroglycerin and, 336, 337 
nitrous oxid and, 389 
normal, 53, 361 

rule for estimating, 360 
in obstetrics, 376 
ocular tension and, 402 
in old age, 252 
in ophthalmology, 402 
opium and, 339 

orthostatic albuminuria and, 191 
pancreas extract and, 279 
in paracentesis abdominalis, 387 
in paratyphoid fever, 206 
in paresis, 375 

para-oxyphenylethylamin and, 333 
in paroxysmal dyspnea, 288 
passive change of posture in, 149 
pediatrics and, 360 
in pericardial effusions, 248 
phlebotomy and, 314 
in phosphorus poisoning, 228 
physical efficiency and, 362 
pituitary extract and, 340 
in pleural effusions, 222 
in pneumonia, 202 
in pneumothorax, 223 
in polycythemia, 297 
postural response in, 146 
posture and, 48 

patient and, 384 
in pregnancy, 396 
at puberty, 361 
in pulmonary edema, 291 

hemorrhage, 219 
pulse, 37 

in pulsus alternans, 243 
purgation and, 302 
quotient, 158 

Barach's formula, 161 

Erlanger and Hooker's for- 
mula, 160 

Fuerst and Soetbeer's for- 
mula, 160 

Strassburger's formula, 159 

von Recklinghausen's for- 
mula, 161 
radio-active substances in, 321 
renal decapsulation and, 323 
respiration and, 38 
in retinal arteries, 402 

hemorrhages, 408 
salvarsan and, 341 
in scarlet fever, 205 
secretion and, 46 

of urine and, 286 
in shock, 210 

treatment of, 211 



Blood-pressure, significance of, 132 
sleep and, 50, 303 
in smallpox, 206 

sodium chloride metabolism and, 
285 
nitrite and, 338 
in spinal anesthesia, 392 
in status lymphaticus, 355 
strophanthus and, 341 
strychnin and, 342 
in surgery, 376 
in surgical hemorrhage, 381 

shock, 378 
hi syphilis, 213 
in syphilitic aortitis, 288 

myocarditis, 242 
in syringomyelia, 375 
systolic, 37 
in tachycardia, 242 

paroxysmal, 242 
testes and, 399 
throughout vascular tree, 23 
thyroid extract and, 343 
tissue extracts and, 351 
in tobacco poisoning, 228 

arteriosclerosis and, 230 
tropical climates and, 359 
in tuberculosis, 213 
in tumors of brain, 372 
in typhoid fever, 206 
in uremia, 287 
ure thane and, 343 
vasotonin and, 343 
venous, 23, 27 

in shock, 380 
visceral manipulations and, 385 
visual accommodation and, 410 
yohimbin and, 344 
Bloodvessels, resistance of, estimation 

of, 173 
Bornstein's method of estimation of 

blood-flow, 170 
Bouloumie's sphygmomanometer, 119 
Bradycardia, blood-pressure hi, 242 
Brain, hemorrhages of, blood-pressure 
in, 372 
tumors of, blood-pressure in, 
372 
Bromides, blood-pressure and, 330 
Bronchial asthma, blood-pressure in, 

249 
Brugsch's sphygmomanometer, 97 
Bussenius's sphygmomanometer, 102 



Cachexia, blood-pressure in, 356 
Caffein, blood-pressure and, 326 
Camphor, blood-pressure and. 327 
Capillaries, physiology of, 29 



INDEX 



417 



( 'apillarv blood-pressure, estimation of, 
140, 175 
pressure, effects of alterations of 
arterial pressure on, 55 
Carcinoma, blood-pressure in, 356 
Cardiac action, venous pressure and, 143 
cycle and blood-pressure, 25 
disease, blood-pressure in, 233 
load, 267 
rate, 27 
tone, 27 
Cardiovascular disease, arterial hyper- 
tension in, 266 
symptoms in arterial hypertension, 
* 270 
Cataract, lenticular, blood-pressure in, 

407 
Cerebral hemorrhages, blood-pressure 
in, 372 
vascular crises, 260 
Cerebrospinal meningitis, blood-press- 
ure in, 202 
pressure in blood-pressure, 372, 
392 
Chemical regulation of blood-pressure, 

33 
Cheyne-Stokes respiration, blood-press- 
ure in, 290 
Chilblains, vascular crises and, 262 
Childhood, blood-pressure in, 360 
Chloral, blood-pressure effect of, 330 
Chlorin gas poisoning, 228 
Chloroform, blood-pressure effect of, 
389 
in pulmonary hemorrhage, 219 
Chlorosis, 356 

Cholera, blood-pressure in, 199 
Christen's energometer, 179 
Circulation, functional efficiency of, 145 
amplitude frequency pro- 
duct of, 161 
Crampton's table of, 146 
energy index in, 161 
Graupner's test of, 151 
Katzenstein's test of, 153 
Claudication, intermittent, in vascular 

crises, 261 
Climate, 359 

Cocain, blood-pressure effect of, 390 
Colic, biliary, in vascular crises, 260 

renal, in vascular crises, 260 
Collapse, blood-pressure in, 210 
Conduction of pulse waves, 124 
Coronary arteries, effect of drugs on, 

344 
Corpulence, 269, 354 
Cramps in the legs, treatment of, 264 
Crampton's table of functional effi- 
ciency of circulation, 146 
Critical venous pressure, 26 
Cuff, blood-pressure, 59 
27 



Decompensation and venous blood- 
pressure, 329 
Delirium tremens, blood-pressure in, 

231 
Dementia precox, blood-pressure in, 

371 
Depressor nerve, physiology of, 31 
Dermographism, vascular crises and, 

262 
Diabetes, blood-pressure in, 347 
Diastole, time relations of, 25 
Diastolic pressure, definition of, 17 
estimation of, 64, 121 
by palpation, 65 
significance of, 130 
by visualization, 65 
Diet, blood-pressure and, 305 

in hypertension, 305 
Digitalis, blood-pressure effect of, 327 
in failing compensation, 328 
in high-pressure stasis, 328 
in pulmonary hemorrhage, 220 
Dilatation, paroxysmal, of abdominal 

aorta, 259 
Diphtheria, blood-pressure in, 199 
Dysmenorrhea and blood-pressure, 396 
Dyspnea, paroxysmal, blood-pressure 

in, 288 
Drugs, effects of, on blood-pressure, 324 
on coronary arteries, 344 
on vasomotor system, 211 
on venous pressure, 345 
Durozier's sign of aortic insufficiency, 

238 
Dynamic diagrams in estimation of 
blood-flow, 179 



E 



Eclampsia, blood-pressure in, 398 
Edema, angioneurotic, vascular crises 
and, 263 
blood-pressure and, 241 
pulmonary, blood-pressure in, 291 
sodium chloride and, 285 
Ehret's phenomenon, 65 
Electricity, blood-pressure and, 315 
Encephalopathy, blood-pressure in, 227 
End-pressure, definition of, 18 
Endocarditis, acute, blood-pressure in, 

234 
Energometer, Christen's, 179 
Energy index in functional efficiency 

of circulation, 161 
Epilepsy, blood-pressure in, 371 
Epinephrin, blood-pressure and, 33, 330 
Ergometer, Zuntz's, 151 
Ergostat, Gaertner's, 151 



418 



INDEX 



Ergot, blood-pressure and, 332 

in pulmonary hemorrhage, 220 

Erlanger and Hooker's formula of 
blood-pressure quotient, 160 

Erlanger's sphygmomanometer, 91 

Erythrol tetranitrate, blood-pressure 
and, 338 

Ether, blood-pressure effect of, 388 

Ethyl chlorid, blood-pressure effect of, 
389 

Exercise, blood-pressure and, 46, 149, 
305, 365 

Exogenous intoxications, blood-press- 
ure in, 225 

Exophthalmic goitre, blood-pressure in, 
352 

Extrasystolic arhythmia, blood-press- 
ure in, 242 

Extra-uterine pregnancy, blood-press- 
ure in, 399 

Eye-grounds in arterial hypertension, 
411 



Fasting, effect on blood-pressure, 306 
Faught's sphygmomanometer, 73 
Fedd6's oscillometer, 105 
Feeding, blood-pressure and, 49 
Fellner's method of estimation of 

blood-flow, 170 
Fevers, blood-flow in, 197 
Fibrillation, auricular, blood-pressure 

in, 243 
Finger plethysmograph, Fleischer's, 168 
Fleischer's finger plethysmograph, 168 

sphygmomanometer, 101 
Fluid intake, blood-pressure and, 308 
Francois Frank's sphygmomanometer, 

118 
Frank and Reh's method of estimation 

of venous pressure, 137 
Frey's method of estimation of venous 

pressure, 136 
Fuerst and Soetbeer's formula of blood- 
pressure quotient, 160 
Function, arterial, estimation of, 173 
Functional capacity of heart, 145 
efficiency of circulation, 145 
hypotension, 233 
tests of arteries, 255 



G 



Gaertner's ergostat, 151 

method of estimation of venous 
pressure, 135 

phenomenon, 135 

sphygmomanometer, 76 
Gastro-enteritis, blood-pressure in, 367 



Gastro-intestinal symptoms of arterial 
hypertension, 270 

Gibson's sphygmomanometer, 88 

Glandular extracts, blood-pressure and, 
351 

Glaucoma, blood-pressure in, 407 

Gonads, effect on blood-pressure, 34, 
399 

Gout, blood-pressure in, 34S 

Graphic method of estimation of blood- 
pressure, 83 

Graupner's test of functional efficiency 
of circulation, 151 



Heart and blood-pressure, 24 

diseases of, blood-pressure in, 233 
effects of alterations of blood-press- 
ure on, 55 
functional capacity of, 145 
symptoms of arterial hypertension, 

271 
work done by, 299 
Hemic viscosity, blood-pressure and, 

297 
Hemiplegia, blood-pressure in, 374 
Hemoglobinuria, vasomotor, 192 
Hemorrhage, blood-pressure in, 355, 

381 
Hemorrhages of brain, blood-pressure 
in, 372 
pulmonary, blood-pressure in, 219 
retinal, blood-pressure in, 408 
surgical, blood-pressure in, 381 
Hertz's sphygmomanometer, 81 
Hewlett's method of estimation of 

blood-flow, 170 
Hill's sphygmomanometer, 72 
Hooker and Eyster's method of estima- 
tion of venous pressure, 137 
Hormonal, blood-pressure and, 334 
Howell's method of estimation of 

venous pressure, 137 
Hurthle's manometer, 20 
Hydrastinin, blood-pressure effects of, 

334 
Hydrastis, blood-pressure effects of, 333 
Hydrotherapy, blood-pressure and, 309 
Hydrothorax, blood-pressure in, 222 
Hyperemesis gravidarum, blood-press- 
ure in, 399 
Hyperglycemia and hypertension, 285, 

347 
Hyperpiesis, 273 
Hypertension, arterial, 299 

bandaging of extremities in, 

315 
in cardiovascular disease, 299 
climate in, 320 



INDEX 



419 



Hypertension, arterial, complications 
of, 287 
conservation of energy in, 

308 
counterirritation in, 319 
diet in, 305 
electricity in, 315 
exercise in, 305 
eye-grounds in, 411 
fluid intake in, 308 
hemic viscosity and, 297 
hydrotherapy in, 309 
massage in, 318 
Nauheim baths in, 309 
phlebotomy in, 314 
prognosis of, 291 
radio-active substances in, 321 
respiratory gymnastics in, 320 
retinal hemorrhages in, 408 
specific treatment in, 213 
surgical treatment in, 323 
symptoms of, 270 
arteries in, 271 
aural, 270 
cardiovascular, 270 
gastro-intestinal, 270 
heart in, 271 
nervous, 270 
ocular, 270 
renal, 270 
signs in, 271 
treatment of, 299 
psychic, 320 
hyperglycemia and, 285, 347 
in nephritis, 272 
etiology of, 274 
symptoms of, 274 
nitrogen retention and, 285 
renal circulation and, 281 

function and, 281 
secretion of urine in, 282 
viscosity and, 297 
Hypnosis, 150 
Hypotension, 185 
causes of, 185 
etiology of, 188 
extreme, prolonged, 356 
functional, 233 
in lumbago, 193 
mechanical, 233 
in myalgia, 193 
in neuritis, 193 
in phosphaturia, 193 
in rheumatoid arthritis, 193 

treatment of, 193 
in sciatica, 193 
in status lymphaticus, 193 
symptoms of, 185 
terminal, 233 

treatment of infectious disease, 
209 



Infectious diseases, blood-pressure in, 
196 
venous pressure in, 198 
Insufficiency, mitral, blood-pressure in, 

239 
Intoxications, exogenous, blood-press- 
ure in, 225 
Intra-abdominal pressure, 41 
estimation of, 183 
increased, 260 
Intracranial blood-pressure, 42 
Intra-ocular blood-pressure, 43 

pressure, venous pressure and, 

404 
tension, estimation of, 405 
Intrapericardial blood-pressure, 41, 248 
Intravenous injection, venous pressure 

and, 144 
Iodids, blood-pressure and, 334 



Jacquet's sphygmotonograph, 87 
Janeway's sphygmomanometer, 72 
Jaundice, blood-pressure in, 349 



E 



Katzenstein's test of functional effi- 
ciency of circulation, 153 
Kidney, decapsulation and blood-press- 
ure, 323 
Kidneys, amyloid disease of, 274, 276 
blood-pressure and, 275, 286 
effects of alteration of blood-press- 
ure on, 56, 282, 286 
nephritis, 274, 276 
tuberculosis of, 274 



Lateral pressure, definition of, 18 
Lead poisoning, blood-pressure in, 225 
Leg, blood-pressure in, in aortic insuffi- 
ciency, 236 
Lenticular cataract, blood-pressure in, 

407 
Life insurance, blood-pressure and, 

359 
Locomotor ataxia, blood-pressure in, 

374 
Lumbago, hypotension in, 193 
Lumbar puncture, blood-pressure in, 

391 
Lymph circulation and in blood-press- 
ure, 34 



420 



INDEX 



M 

Malaria, blood-pressure in, 201 
Malingering, detection of, 369 
Mannitol nitrate, blood-pressure effect 

of, 338 
Manometer, Hiirthle's, 20 
maximum, 21 
mercury, 19 
minimum, 21 
(see sphygmomanometer) 
Manometers, spring, in estimation of 

venous pressure, 135 
Massage, blood-pressure and, 318 
Mean pressure, definition of, 17 

rule for estimating, 37 
Mechanical hypotension, 233 
Meningitis, cerebrospinal, blood-press- 
ure in, 202 
tuberculous, blood-pressure in, 202 
Menopause, blood-pressure in, 396 
Menstruation, blood-pressure during, 

395 
Mental diseases, blood-pressure in, 
370 
work, physiology of, 31 
Mercer's sphygmomanometer, 72 
Mercurial poisoning, blood-pressure in, 

296 
Mercury manometer, 19 
Metabolic diseases, blood-pressure in, 

347 
Metabolism, sodium chloride, blood- 
pressure and, 285 
Mistletoe, blood-pressure and, 336 
Mitral insufficiency, blood-pressure in, 
239 
obstruction, blood-pressure in, 240 
stenosis, blood-pressure in, 241 
Momburg's belt constriction, 393 
Moritz and Tabora, intravenous needle 
of, in estimation of venous pressure, 
138 
Moritz 's method of estimating intra- 
abdominal pressure, 183 
Morphin, blood-pressure and, 339 
Morphinism, blood-pressure in, 232 
Muenzer's sphygmomanometer, 99 
Muscular exertion in blood-pressure, 

46, 149, 305, 365 
Myalgia, hypotension in, 193 
Myocarditis, syphilitic, 242 
Myocardium, blood-pressure in diseases 

of, 241 
Myxedema, blood-pressure in, 354 



N 



Nauheim baths, blood-pressure efforts 
of, 309 



Neosalvarsan, effect on blood-pressure, 

342 
Nephritis, acute, blood-pressure in, 
296 
chronic, blood-pressure in, 272 
hypertension in, 272 
Nerve, depressor, physiology of, 31 
Nervous symptoms of arterial hyper- 
tension, 270 
system, diseases of, blood-pressure 
in, 369 
Neurasthenia, blood-pressure in, 369 
Neuritis, hypotension in, 193 
Neuroses, blood-pressure in, 369 
Nicholson's sphygmomanometer, 71 
Nitrite test of arteriosclerosis, 254 
Nitrites, blood-pressure and, 336 

in pulmonary hemorrhage, 220 
Nitrogen- retention and blood-pressure, 

285, 286 
Nitroglycerin, blood-pressure effects of, 

336, 337 
Nitrous oxid, blood-pressure and, 389 
Normal arterial blood-pressure, 53, 361 
venous blood-pressure, 141 



Obstetrics, blood-pressure in, 376 
Obstruction, aortic, blood-pressure in, 
238 
mitral, blood-pressure in, 240 
Ocular sphygmomanometer, Bajardi's, 
403 
Rubino's, 403 
symptoms of arterial hypertension, 
270 
Oliver's sphygmomanometer, 79 
Ophthalmology, blood-pressure in, 402 
Opium, blood-pressure and, 339 
Orthostatic albuminuria, 191 

blood-pressure and, 191 
Oscillations of first order, 17 
of second order, 17 
of third order, 18 
Oscillatory method of estimation of 

blood-pressure, 102 
Oscillometer, Fedde's, 105 
Ovaries and vasomotor reactions, 396 



Pachon's sphygmomanometer, 10S 
Palpatory estimation of blood-pressure, 

62 
Pal's sphygmoscope, 107 
Pancreas extract, effect on blood-press- 
ure, 279 



INDEX 



421 



Paracentesis abdominalis, blood-press- 
ure effects of, 387 
Paratyphoid fever, blood-pressure in, 

206 
Paresis, blood-pressure in, 375 
Para-oxyphenylethylamin, blood-press- 
ure and, 333 
Paroxysmal dilatation of abdominal 
aorta, 259 
dyspnea, blood-pressure in, 28S 
tachycardia, blood-pressure in, 
242 
Pediatrics, blood-pressure and, 3G0 
Pelvic viscera, manipulations of, and 

blood-pressure, 386 
Periarteritis nodosa, 354 
Pericardial effusions, blood-pressure in, 

41, 248 
Phenomenon, Gaertner's, 135 
Phlebotomy, blood-pressure and, 219, 

314, 376 
Phosphaturia, hypotension in, 193 
Phosphorous poisoning, blood-pressure 

in, 228 
Physical efficiency and blood-pressure, 

362 
Physiology of arteries, 28 
of arterioles, 29 
of capillaries, 29 
of depressor nerve, 31 
of mental work, 31 
of vasoconstrictor system, 29 
of vasodilator nerves, 32 

system, 32 
of vasomotor system, 29 
of veins, 29 
Pilocarpin, 340 
Pituitary extract, blood-pressure and, 

340 
Pituitrin in pulmonary hemorrhage, 

220 
Plethysmograph in estimation of blood- 
flow, 166 
Fleischer's finger, 168 
Pleura, aspiration of, effect on blood- 
pressure, 386 
Pleural effusions, blood-pressure in, 

222 
Pneumonia, blood-pressure in, 202 
Pneumothorax, blood-pressure in, 223 
Poisoning, arsenic, blood-pressure in, 
228 
lead, blood-pressure in, 225 
mercurial, blood-pressure in, 296 
phosphorus, blood-pressure in, 228 
tobacco, blood-pressure in, 288 
Polycythemia, blood-pressure in, 297 
Postural response in blood-pressure, 

146 
Posture, blood-pressure and, 48 
Potain's sphygmomanometer, 118 



Pregnancy, blood-pressure and vis- 
cosity, 298 
extra-uterine, blood-pressure in, 

399 
normal, blood-pressure in, 396 
Pressure, diastolic, definition of, 17 
lateral, definition of, 18 
mean, definition of, 17 
estimation of, 37 
normal, 53, 361 
pulse, definition of, 17 
systolic, definition of, 17 
venous, 135 
Puberty and blood-pressure, 361 
Pulmonary edema, blood-pressure in, 
291 
hemorrhage, blood-pressure in, 219 
chloroform in, 220 
digitalis in, 220 
ergot in, 220 
nitrites in, 220 
pituitrin in, 220 
treatment of, 219 
pressure, effects of alterations of 
blood-pressure on, 55 
Pulse, blood-pressure and, 37, 246 
deficit, 243 
pressure, definition of, 17 

urinary secretion and, 282, 

286 
range of, 38 
significance of, 132 
waves, conduction of, 124 
Pulsus alternans, blood-pressure in, 243 

paradoxus, 189, 249 
Purgation, blood-pressure and, 302 



R 



Radio-active substances effect on 

blood-pressure, 321 
Reflex, ocular, 412 

Renal circulation, hypertension and, 
281 
colic in vascular crises, 260 
function, blood-flow and, 281 

hypertension and, 281 
symptoms in arterial hypertension, 
270 
Respiration, blood-pressure and, 3S 
Cheyne-Stokes, blood-pressure in, 

290 
venous pressure and, 143 
Retinal arteries, blood-pressure in, 402 
pulsation of, 409 
spasm of, 409 
hemorrhages, blood-pressure in, 40S 
Rheumatoid arthritis, hypotension in, 
193 



422 



INDEX 



Riva-Rocci type of sphygmomanom- 
eter, 62 

Rubino's ocular sphygmomanometer, 
403 



Sahxi's sphygmobolometer, 178 

Salvarsan, blood-pressure and, 341 

Scarlet fever, blood-pressure in, 205 

Schiotz's tonometer, 405 

Schott's test by venous pressure, 155 

Sciatica, hypotension in, 193 

Scurvy, 355 

Secretion, blood-pressure and, 46 

Shock, blood-pressure in, 210, 378 

medical or toxic, 210 
Significance of blood-pressure changes, 

130 
Silbermann's sphygmomanometer, 96 
Singer's sphygmomanometer, 91 
Sleep, blood-pressure and, 50, 303 
Smallpox, blood-pressure in, 206 
Sodium chloride, edema and, 286 

metabolism, blood-pressure 
and, 285 

nitrite, blood-pressure and, 338 
Spasm of retinal arteries, 409 
Sphygmobolometer, 175 
Sphygmogram, absolute, in blood-press- 

.ure, 156 
Sphygmomanometer, aneroid, 108 
standardization of, 115 

classification of, 133 

compressed-air, 79 

Bendick's, 82 

Bing's, 106 

Bishop's, 79 

Bouloumie's, 119 

Brugsch's, 97 

Bussenius's, 102 

Erlanger's, 91 

Faught's, 73 

Fleischer's, 101 

Francois Frank's, US 

Gaertner's, 76 

Gibson's, 88 

Hertz's, 81 

Hill's, 72 

Janeway's, 72 

McKeson's, 400 

Mercer's, 72 

Muenzer's, 99 

Nicholson's, 71 

ocular, Bajardi's, 403 
Rubino's, 403 

Oliver's, 79 

Pachon's, 10S 

Potain's, 118 

Riva-Rocci type of, 62 

Silbermann's, 96 



Sphygmomanometer, Singer's, 91 
Stanton's, 63 
Tycos, 112 
Uskoff's, 93 
Van Westenrijk's, 79 
Vaquez's, 108 
von Recklinghausen's, 115 
Widmer's, 106 
Wybauw's, 102 
Sphygmomanometers, comparative 

values of, 120 
Sphygmoscope, Pal's, 107 
Sphygmotonograph, Jaequet's, 87 
Spinal anesthesia, blood-pressure in, 

392 
Standardization of aneroid sphygmo- 
manometer, 115 
Stanton's sphygmomanometer, 63 
Stasis, high pressure, 234, 268, 314, 328 

digitalis in, 328 
Status lymphaticus, blood-pressure in, 
355 
hypotension in, 193 
Stephenson's tonometer, 406 
Stewart's method of estimation of 

blood-flow, 163 
Strassburger's formula of blood-press- 
ure quotient, 159 
Strophanthus, blood-pressure effect of, 

341 
Strychnin, blood-pressure effect of, 342 
Subjective method of estimation of 

blood-pressure, 119 
Suckling, effect of, on blood-pressure, 

361 
Suprarenal glands, physiology, 33, 280, 

330 
Surgery, blood-pressure in, 376 
Surgical hemorrhage, blood-pressure in, 
381 
shock, blood-pressure in, 378 
treatment of, 382 
Syphilis, blood-pressure in, 213 
Syphilitic aortitis, blood-pressure in, 

235, 288 
Syringomyelia, blood-pressure in, 375 
Systole, time relations of, 25 
Systolic blood-pressure, 37 
output, 26, 130 
pressure, definition of, 17 
estimation of, 62 



Tache cerebrale, 263 
Tachograph in estimation of blood- 
flow, 171 
von Ivries's, 172 
Tachycardia, blood-pressure in, 242 
Terminal hypotension, 233 



INDEX 



423 



Testes, effect of, on blood-pressure, 399 
Thoracentesis, effect of, on blood-press- 
ure, 386 
Thoracic viscera, manipulations of, and 

blood-pressure, 386 
Thyroid extract, blood-pressure and, 

343 
Tissue extracts, blood-pressure and, 351 
Tobacco poisoning, blood-pressure in, 

228 
Tonometer, Schiotz's, 405 

Stephenson's, 406 
Tonus, arterial, estimation of, 174 
Toxemia, alimentary, 350 
Training, effect of, on blood-pressure, 

367 
Traube-Herring waves, 41 
Traube's sign in aortic insufficiency, 

238 
Tropical climates, blood-pressure and, 

359 
Tuberculosis, blood-pressure in, 213 

of kidney, 274 
Tuberculous meningitis, blood-pressure 

in, 202 
Tumors of brain, blood-pressure in, 372 
Tycos sphygmomanometer, 112 
Tympanites in vascular crises, 260 
Typhoid fever, blood-pressure in, 206 
Tyramin, blood-pressure effect of, 194 



Uranium nephritis, blood-pressure in, 

285 
Uremia, blood-pressure in, 287 

lumbar puncture in, 302 

venesection in, 302 
Urethane, blood-pressure and, 343 
Urine, secretion of, blood-pressure and, 
286 

' in hypertension, 282 
Urticaria, vascular crises and, 262 
Uskoff's sphygmomanometer, 93 



Van Westenrijk's sphygmomanom- 
eter, 79 
Van Zwaluwenburg's method of estima- 
tion of blood-flow, 170 
Vaquez's sphygmomanometer, 108 
Vascular crises, 256 

angina abdominalis in, 259 

pectoris in, 257 
angioneurotic edema and, 263 
apoplexy in, 261 
biliary colic in, 260 
cerebral, 260 
chilblains and, 262 



Vascular crises in children, 263 
compensation, 271 
dermographism and, 262 
epilepsy and, 260, 371 
intermittent claudication in, 

261 
in locomotor ataxia, 374 
peripheral, 261 
renal colic in, 260 
treatment of, 264 
tympanites in, 260 
urticaria and, 262 
vasoconstriction and, 257 
vertigo in, 261 
reactions in arteriosclerosis, 252 
tree, blood-pressure throughout, 
23 
Vasoconstriction, vascular crises and, 

257 
Vasoconstrictor system, physiology of, 

29 
Vasodilator nerves, physiology of, 32 
system, physiology of, 32 
therapeusis, 211 
Vasomotor efficiency test, 146 
system, physiology of, 29 
Vasotonin, blood-pressure and, 343 
Veins, physiology of, 29 
Venesection, effect on blood-pressure, 
314, 376 
in uremia, 302 
Venous blood-pressure, 23, 27, 135 
cardiac action and, 143 
critical, 26 

effect of drugs on, 345 
effects of alterations of blood- 
pressure on, 55 
estimation of blood-flow, sys- 
tolic output by, 164 
Frank and Reh's method, 
137 
• Frey's method, 136 
Gaertner's method, 135 
Hooker and Eyster's 

method, 137 
Howell's method, 137 
intravenous needle of 
Moritz and Tabora in, 
138 
spring manometers in, 
135 
factors influencing, 141 
in infectious diseases, 198 
intra-ocular pressure and, 404 
intravenous injection and, 

144 
in nephritis, 285 
respiration and, 143 
Schott's test of, 155 
Veratrum viride, 344, 398 
Vertigo in vascular crises, 261 



424 



INDEX 



Visceral manipulations and blood-press- 
ure, 385 
Viscosity of blood, 35 
in pregnancy, 298 
and hypertension, 297 
Visual accommodation, blood-pressure 
and, 410 
method of estimation of blood- 
pressure, 102 
Vries-Reilingh's method of estimation 

of arterial tonus, 174 
Von Kries's tachograph, 172 
Von Recklinghausen's formula of blood- 
pressure quotient, 161 
sphygmomanometer, 115 
Vomiting, blood-pressure during, 329, 
372 



Vomiting, dangers of, 329 

of pregnancy and blood-pressure, 
399 

W. 

White line of adrenal insufficiency, 263 
Widmer's sphygmomanometer, 106 



Yohimbin, blood-pressure effect of, 344 



Zuntz's ergometer, 151 






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